DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys
Identifieur interne : 002080 ( Istex/Corpus ); précédent : 002079; suivant : 002081DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys
Auteurs : A. L. Lobashevsky ; P. X. Wang ; J. F. George ; J. Contreras ; J. Townsend ; J. M. ThomasSource :
- Human Immunology [ 0198-8859 ] ; 1998.
English descriptors
- KwdEn :
- Teeft :
- Allele, Allogeneic, Allogeneic stimulation, Allograft, Allograft acceptance, Allograft rejection, Alloimmune responses, Allostimulation, American society, Assay, Autostimulated culture, Cell proliferation, Cell surface, Chain genes, Curr opin immunol, Cytokine, Cytokine prevalence, Cytokine production, Cytokine profile, Cytokine profiles, Cytokine response, Cytokine responses, Dendritic, Dendritic cells, Different patterns, Drb1, Early studies, Elispot, Elsevier science, Further study, Gene products, Graft, Graft rejection, Grand island, High number, Histocompatibility, Human immunol, Human immunology, Immunol, Immunol today, Immunological methods, Leukoc biol, Lobashevsky, Lymphocyte, Lymphocyte reaction, Macaque, Macaque model, Major histocompatibility, Mismatch, Molecular typing, Multiple drb1, Nonhuman primates, Normal monkey serum, Peripheral blood, Positive control, Preclinical studies, Primary alloimmune responses, Primary structure, Primates, Primer, Proc natl acad, Proinflammatory, Proliferative response, Relative response, Rhesus, Rhesus macaques, Rhesus monkeys, Significant correlation, Significant difference, Significant effect, Single cell level, Statistical analysis, Stimulation index, Transplant, Transplant center, Transplant proc, Transplant recipients, Transplantation, Transplantation immunity, Tumor necrosis, Type cytokine production, Unrelated combinations, Various numbers.
Abstract
Abstract: Human and nonhuman primates have multiple DR B1 and non-B1 alleles. However, the role of mismatched DR non-B1 alleles in primary alloimmune responses is not well understood. Macaques, which share close DNA homologies with human MHC genes and have a high number of β-chain genes in the DR subregion, are preeminent preclinical models for immunologic studies of transplant tolerance and immunosuppression. In this study, we examined the effect of allogeneic MHC Class II DRB mismatches in Th1- and Th2-like cytokine responses elicited in one-way MLR cultures in rhesus macaques. An ELISPOT method was used to estimate cytokine secretion at the single cell level. Molecular typing for DRB1 and DR non-B1 alleles was performed by a moderate-high resolution PCR-SSP method using a panel of 55 primer pairs covering 74 DRB alleles and clusters. Of 35 unrelated combinations, 66% had multiple (≥2) allelic MM at DRB1 and DR non-B1 with no significant correlation between numbers of DRB1 and DR non-B1 mismatches. Pairs with 1 or 0 MM were assigned to a mono/null MM group to obtain sufficient numbers for statistical analysis. The pairs differing by multiple vs. mono/null DRB1 MM showed no significant difference in cytokine prevalence (P = 0.69). In contrast, high IFN-γ/IL4 SFC ratios were noted in pairs with multiple vs. mono/null DR non-B1 MM (p = 0.0009). IFN-γ/IL-10 spot forming cell (SFC) ratios were consistent with IFN-γ/IL-4 SFC ratios (r = 0.98). Multiple DR non-B1 mismatches showed a trend towards higher MLR proliferative responses, although the stimulation index did not reflect the dominant cytokine response. These observations suggest a bias towards Th1-like cytokine production under allostimulation with multiple DR non-B1 gene products. Further study of the primary structure of DR non-B1 determinants may be helpful in understanding the fine molecular mechanisms governing the regulation of cytokine profiles during allostimulation in primates.
Url:
DOI: 10.1016/S0198-8859(98)00024-X
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title><author><name sortKey="Lobashevsky, A L" sort="Lobashevsky, A L" uniqKey="Lobashevsky A" first="A. L." last="Lobashevsky">A. L. Lobashevsky</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Wang, P X" sort="Wang, P X" uniqKey="Wang P" first="P. X." last="Wang">P. X. Wang</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="George, J F" sort="George, J F" uniqKey="George J" first="J. F." last="George">J. F. George</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Contreras, J" sort="Contreras, J" uniqKey="Contreras J" first="J." last="Contreras">J. Contreras</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Townsend, J" sort="Townsend, J" uniqKey="Townsend J" first="J." last="Townsend">J. Townsend</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Thomas, J M" sort="Thomas, J M" uniqKey="Thomas J" first="J. M." last="Thomas">J. M. 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Thomas, UAB Transplant Center, Boshell Diabetes Building 802, 1808 7th Street South, Birmingham, AL 35294-0012</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jthomas@uab.edu</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DA4A6943CC5129B5ED61A11C7AACFFF93A2C008C</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1016/S0198-8859(98)00024-X</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-L7WBN221-S/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002080</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002080</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title><author><name sortKey="Lobashevsky, A L" sort="Lobashevsky, A L" uniqKey="Lobashevsky A" first="A. L." last="Lobashevsky">A. L. Lobashevsky</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Wang, P X" sort="Wang, P X" uniqKey="Wang P" first="P. X." last="Wang">P. X. Wang</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="George, J F" sort="George, J F" uniqKey="George J" first="J. F." last="George">J. F. George</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Contreras, J" sort="Contreras, J" uniqKey="Contreras J" first="J." last="Contreras">J. Contreras</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Townsend, J" sort="Townsend, J" uniqKey="Townsend J" first="J." last="Townsend">J. Townsend</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation></author><author><name sortKey="Thomas, J M" sort="Thomas, J M" uniqKey="Thomas J" first="J. M." last="Thomas">J. M. Thomas</name><affiliation><mods:affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Address reprint requests to: Dr. Judith M. Thomas, UAB Transplant Center, Boshell Diabetes Building 802, 1808 7th Street South, Birmingham, AL 35294-0012</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jthomas@uab.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Immunology</title><title level="j" type="abbrev">HIM</title><idno type="ISSN">0198-8859</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">59</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="363">363</biblScope><biblScope unit="page" to="372">372</biblScope></imprint><idno type="ISSN">0198-8859</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0198-8859</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ELISPOT</term><term>MHC</term><term>MLR</term><term>MM</term><term>NMS</term><term>RR</term><term>SFC</term><term>SI</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Allele</term><term>Allogeneic</term><term>Allogeneic stimulation</term><term>Allograft</term><term>Allograft acceptance</term><term>Allograft rejection</term><term>Alloimmune responses</term><term>Allostimulation</term><term>American society</term><term>Assay</term><term>Autostimulated culture</term><term>Cell proliferation</term><term>Cell surface</term><term>Chain genes</term><term>Curr opin immunol</term><term>Cytokine</term><term>Cytokine prevalence</term><term>Cytokine production</term><term>Cytokine profile</term><term>Cytokine profiles</term><term>Cytokine response</term><term>Cytokine responses</term><term>Dendritic</term><term>Dendritic cells</term><term>Different patterns</term><term>Drb1</term><term>Early studies</term><term>Elispot</term><term>Elsevier science</term><term>Further study</term><term>Gene products</term><term>Graft</term><term>Graft rejection</term><term>Grand island</term><term>High number</term><term>Histocompatibility</term><term>Human immunol</term><term>Human immunology</term><term>Immunol</term><term>Immunol today</term><term>Immunological methods</term><term>Leukoc biol</term><term>Lobashevsky</term><term>Lymphocyte</term><term>Lymphocyte reaction</term><term>Macaque</term><term>Macaque model</term><term>Major histocompatibility</term><term>Mismatch</term><term>Molecular typing</term><term>Multiple drb1</term><term>Nonhuman primates</term><term>Normal monkey serum</term><term>Peripheral blood</term><term>Positive control</term><term>Preclinical studies</term><term>Primary alloimmune responses</term><term>Primary structure</term><term>Primates</term><term>Primer</term><term>Proc natl acad</term><term>Proinflammatory</term><term>Proliferative response</term><term>Relative response</term><term>Rhesus</term><term>Rhesus macaques</term><term>Rhesus monkeys</term><term>Significant correlation</term><term>Significant difference</term><term>Significant effect</term><term>Single cell level</term><term>Statistical analysis</term><term>Stimulation index</term><term>Transplant</term><term>Transplant center</term><term>Transplant proc</term><term>Transplant recipients</term><term>Transplantation</term><term>Transplantation immunity</term><term>Tumor necrosis</term><term>Type cytokine production</term><term>Unrelated combinations</term><term>Various numbers</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Human and nonhuman primates have multiple DR B1 and non-B1 alleles. However, the role of mismatched DR non-B1 alleles in primary alloimmune responses is not well understood. Macaques, which share close DNA homologies with human MHC genes and have a high number of β-chain genes in the DR subregion, are preeminent preclinical models for immunologic studies of transplant tolerance and immunosuppression. In this study, we examined the effect of allogeneic MHC Class II DRB mismatches in Th1- and Th2-like cytokine responses elicited in one-way MLR cultures in rhesus macaques. An ELISPOT method was used to estimate cytokine secretion at the single cell level. Molecular typing for DRB1 and DR non-B1 alleles was performed by a moderate-high resolution PCR-SSP method using a panel of 55 primer pairs covering 74 DRB alleles and clusters. Of 35 unrelated combinations, 66% had multiple (≥2) allelic MM at DRB1 and DR non-B1 with no significant correlation between numbers of DRB1 and DR non-B1 mismatches. Pairs with 1 or 0 MM were assigned to a mono/null MM group to obtain sufficient numbers for statistical analysis. The pairs differing by multiple vs. mono/null DRB1 MM showed no significant difference in cytokine prevalence (P = 0.69). In contrast, high IFN-γ/IL4 SFC ratios were noted in pairs with multiple vs. mono/null DR non-B1 MM (p = 0.0009). IFN-γ/IL-10 spot forming cell (SFC) ratios were consistent with IFN-γ/IL-4 SFC ratios (r = 0.98). Multiple DR non-B1 mismatches showed a trend towards higher MLR proliferative responses, although the stimulation index did not reflect the dominant cytokine response. These observations suggest a bias towards Th1-like cytokine production under allostimulation with multiple DR non-B1 gene products. Further study of the primary structure of DR non-B1 determinants may be helpful in understanding the fine molecular mechanisms governing the regulation of cytokine profiles during allostimulation in primates.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>cytokine</json:string><json:string>mismatch</json:string><json:string>drb1</json:string><json:string>allele</json:string><json:string>immunol</json:string><json:string>transplantation</json:string><json:string>rhesus</json:string><json:string>cytokine production</json:string><json:string>macaque</json:string><json:string>allogeneic</json:string><json:string>allograft</json:string><json:string>lymphocyte</json:string><json:string>histocompatibility</json:string><json:string>proinflammatory</json:string><json:string>elispot</json:string><json:string>allostimulation</json:string><json:string>dendritic</json:string><json:string>lobashevsky</json:string><json:string>primer</json:string><json:string>lymphocyte reaction</json:string><json:string>major histocompatibility</json:string><json:string>cytokine response</json:string><json:string>gene products</json:string><json:string>cytokine profiles</json:string><json:string>dendritic cells</json:string><json:string>cytokine responses</json:string><json:string>stimulation index</json:string><json:string>unrelated combinations</json:string><json:string>peripheral blood</json:string><json:string>grand island</json:string><json:string>nonhuman primates</json:string><json:string>single cell level</json:string><json:string>primates</json:string><json:string>graft</json:string><json:string>assay</json:string><json:string>transplant</json:string><json:string>various numbers</json:string><json:string>statistical analysis</json:string><json:string>relative response</json:string><json:string>human immunol</json:string><json:string>significant difference</json:string><json:string>allogeneic stimulation</json:string><json:string>transplant recipients</json:string><json:string>rhesus macaques</json:string><json:string>graft rejection</json:string><json:string>allograft rejection</json:string><json:string>rhesus monkeys</json:string><json:string>proliferative response</json:string><json:string>transplantation immunity</json:string><json:string>chain genes</json:string><json:string>allograft acceptance</json:string><json:string>human immunology</json:string><json:string>alloimmune responses</json:string><json:string>preclinical studies</json:string><json:string>type cytokine production</json:string><json:string>american society</json:string><json:string>molecular typing</json:string><json:string>elsevier science</json:string><json:string>cytokine prevalence</json:string><json:string>primary alloimmune responses</json:string><json:string>autostimulated culture</json:string><json:string>positive control</json:string><json:string>immunological methods</json:string><json:string>multiple drb1</json:string><json:string>normal monkey serum</json:string><json:string>high number</json:string><json:string>cell proliferation</json:string><json:string>transplant center</json:string><json:string>significant effect</json:string><json:string>cell surface</json:string><json:string>macaque model</json:string><json:string>different patterns</json:string><json:string>significant correlation</json:string><json:string>further study</json:string><json:string>primary structure</json:string><json:string>proc natl acad</json:string><json:string>curr opin immunol</json:string><json:string>tumor necrosis</json:string><json:string>leukoc biol</json:string><json:string>transplant proc</json:string><json:string>immunol today</json:string><json:string>early studies</json:string><json:string>cytokine profile</json:string></teeft></keywords><author><json:item><name>A.L. Lobashevsky</name><affiliations><json:string>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</json:string></affiliations></json:item><json:item><name>P.X. Wang</name><affiliations><json:string>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</json:string></affiliations></json:item><json:item><name>J.F. George</name><affiliations><json:string>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</json:string></affiliations></json:item><json:item><name>J. Contreras</name><affiliations><json:string>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</json:string></affiliations></json:item><json:item><name>J. Townsend</name><affiliations><json:string>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</json:string></affiliations></json:item><json:item><name>J.M. Thomas</name><affiliations><json:string>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</json:string><json:string>Address reprint requests to: Dr. Judith M. Thomas, UAB Transplant Center, Boshell Diabetes Building 802, 1808 7th Street South, Birmingham, AL 35294-0012</json:string><json:string>E-mail: jthomas@uab.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>MLR : mixed lymphocyte reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MHC : major histocompatibility complex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>NMS : normal monkey serum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SI : stimulation index</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RR : relative response</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ELISPOT : enzyme linked immunospot</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SFC : spot forming cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MM : mismatches</value></json:item></subject><arkIstex>ark:/67375/6H6-L7WBN221-S</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Human and nonhuman primates have multiple DR B1 and non-B1 alleles. However, the role of mismatched DR non-B1 alleles in primary alloimmune responses is not well understood. Macaques, which share close DNA homologies with human MHC genes and have a high number of β-chain genes in the DR subregion, are preeminent preclinical models for immunologic studies of transplant tolerance and immunosuppression. In this study, we examined the effect of allogeneic MHC Class II DRB mismatches in Th1- and Th2-like cytokine responses elicited in one-way MLR cultures in rhesus macaques. An ELISPOT method was used to estimate cytokine secretion at the single cell level. Molecular typing for DRB1 and DR non-B1 alleles was performed by a moderate-high resolution PCR-SSP method using a panel of 55 primer pairs covering 74 DRB alleles and clusters. Of 35 unrelated combinations, 66% had multiple (≥2) allelic MM at DRB1 and DR non-B1 with no significant correlation between numbers of DRB1 and DR non-B1 mismatches. Pairs with 1 or 0 MM were assigned to a mono/null MM group to obtain sufficient numbers for statistical analysis. The pairs differing by multiple vs. mono/null DRB1 MM showed no significant difference in cytokine prevalence (P = 0.69). In contrast, high IFN-γ/IL4 SFC ratios were noted in pairs with multiple vs. mono/null DR non-B1 MM (p = 0.0009). IFN-γ/IL-10 spot forming cell (SFC) ratios were consistent with IFN-γ/IL-4 SFC ratios (r = 0.98). Multiple DR non-B1 mismatches showed a trend towards higher MLR proliferative responses, although the stimulation index did not reflect the dominant cytokine response. These observations suggest a bias towards Th1-like cytokine production under allostimulation with multiple DR non-B1 gene products. Further study of the primary structure of DR non-B1 determinants may be helpful in understanding the fine molecular mechanisms governing the regulation of cytokine profiles during allostimulation in primates.</abstract><qualityIndicators><score>10</score><pdfWordCount>5251</pdfWordCount><pdfCharCount>33489</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>585 x 783 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>303</abstractWordCount><abstractCharCount>1972</abstractCharCount><keywordCount>8</keywordCount></qualityIndicators><title>DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title><pmid><json:string>9634198</json:string></pmid><pii><json:string>S0198-8859(98)00024-X</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Human Immunology</title><language><json:string>unknown</json:string></language><publicationDate>1998</publicationDate><issn><json:string>0198-8859</json:string></issn><pii><json:string>S0198-8859(00)X0041-9</json:string></pii><volume>59</volume><issue>6</issue><pages><first>363</first><last>372</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1998</json:string></date><geogName></geogName><orgName><json:string>BioSource International</json:string><json:string>UAB Transplant Center</json:string><json:string>Division of Transplantation Immunology</json:string><json:string>QIAGEN Inc.</json:string><json:string>Murex Diagnostic LTD., UK</json:string><json:string>Department of Surgery and Transplant</json:string><json:string>Vector Laboratories, Inc.</json:string><json:string>Moss Inc., Pasadena</json:string><json:string>American Society</json:string><json:string>Milliport Co.</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>J. F. George</json:string><json:string>Judith M. Thomas</json:string><json:string>J. Contreras</json:string><json:string>Non</json:string><json:string>Data</json:string><json:string>Nat Borden</json:string><json:string>R. Steinman</json:string><json:string>Dana Willis</json:string><json:string>J. Townsend</json:string><json:string>A. L. Lobashevsky</json:string><json:string>P. X. Wang</json:string></persName><placeName><json:string>Birmingham</json:string><json:string>San Diego</json:string><json:string>Chatsworth</json:string><json:string>Finland</json:string><json:string>Wilmington</json:string><json:string>Turku</json:string><json:string>Japan</json:string><json:string>DE</json:string><json:string>Tokyo</json:string><json:string>CA</json:string><json:string>MA</json:string><json:string>AL</json:string><json:string>Cambridge</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[4]</json:string><json:string>[23]</json:string><json:string>A. Lobashevsky et al.</json:string><json:string>[44]</json:string><json:string>Slierendregt et al. [34]</json:string><json:string>[39]</json:string><json:string>[17, 18]</json:string><json:string>[1]</json:string><json:string>[49]</json:string><json:string>[3]</json:string><json:string>[46, 47]</json:string><json:string>[5]</json:string><json:string>Histocompatibility and Immunogenetics, 1998</json:string><json:string>[48]</json:string><json:string>Trinchieri et al.</json:string><json:string>[52]</json:string><json:string>[14, 16]</json:string><json:string>Lobashevsky et al.</json:string><json:string>[31, 32]</json:string><json:string>[40]</json:string><json:string>[2]</json:string><json:string>[11, 20, 21]</json:string><json:string>[19]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-L7WBN221-S</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - immunology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - immunology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - General Medicine</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Immunology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Immunology and Allergy</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1016/S0198-8859(98)00024-X</json:string></doi><id>DA4A6943CC5129B5ED61A11C7AACFFF93A2C008C</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L7WBN221-S/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L7WBN221-S/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-L7WBN221-S/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1998 American Society for Histocompatibility and Immunogenetics</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1998</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>Supported by NIH grants #ROI AII22293 and ROI AI39793.</note><note type="content">Section title: Original Articles</note><note type="content">FIGURE 1: MHC class II typing of representative animal. DRB1∗0309, DRB1∗0403/05, DRB1∗1006, DRB1∗1002/04; DRB3∗0402/05; DRB5∗0301/02/04; DRB6∗0101, DRB6∗0103; DRBw101; DRBw201; DRBw701. PCR products were size separated on 2% agarose gel containing 0.5 μg/ml of ethidium bromide. The entire medium/high resolution-typing panel consisted of 55 allele specific primer mixtures. The name of the amplified allele(s) is given above each lane giving positive signal. The arrows indicate the migration of the 430-bp globin internal positive control and allele specific PCR products varying from 120 to 250 bp.</note><note type="content">FIGURE 2: Distribution of DRB1 and DR non-B1 mismatches in random unrelated responder/stimulator combinations. The animals were DNA typed for DRB locus using PCR-SSP. Groupings were based on the numbers of mismatched DRB alleles. Open sectors correspond to donor/recipient combinations with 0 DRB MM; black sectors correspond to donor/recipient combinations with 1 DRB MM; hatched sectors correspond to donor/recipient combinations with multiple (2–6) DRB MM. The numbers of unrelated combinations of responder/stimulator are: for DRB1 alleles multiple mismatches—23, 1 mismatch—11, 0 mismatches—1; for DR non B1 alleles, multiple mismatches—10, 1 mismatch—3, 0 mismatches—2.</note><note type="content">FIGURE 3: Influence of DR non-B1 incompatibilities on Th1/Th2-like response. Responder T cells were allostimulated with irradiated donor PBMC differing by various numbers of DRB1 and DR non-B1 specificities.</note><note type="content">FIGURE 4: Influence of multiple DR non-B1 MM on T cell alloproliferative responses. The results, which represent the mean value of triplicates, were expressed by the stimulation index (SI) or relative response (RR).</note><note type="content">FIGURE 5: Kinetics of IFN-γ production in serum of kidney recipients which were transplanted with organs differing by various numbers of DR non-B1 MM. One animal was 6 DR non-B1 MM with the donor, 2 animals were 3 DR non-B1 MM with their donors and one animal was 0 DR non-B1 MM with the donor. Monkey serum samples were tested on 3, 4 and 14 days after surgery using ELISA.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title><author xml:id="author-0000"><persName><forename type="first">A.L.</forename><surname>Lobashevsky</surname></persName><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">P.X.</forename><surname>Wang</surname></persName><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">J.F.</forename><surname>George</surname></persName><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">J.</forename><surname>Contreras</surname></persName><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">J.</forename><surname>Townsend</surname></persName><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation></author><author xml:id="author-0005"><persName><forename type="first">J.M.</forename><surname>Thomas</surname></persName><email>jthomas@uab.edu</email><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><affiliation>Address reprint requests to: Dr. Judith M. Thomas, UAB Transplant Center, Boshell Diabetes Building 802, 1808 7th Street South, Birmingham, AL 35294-0012</affiliation></author><idno type="istex">DA4A6943CC5129B5ED61A11C7AACFFF93A2C008C</idno><idno type="ark">ark:/67375/6H6-L7WBN221-S</idno><idno type="DOI">10.1016/S0198-8859(98)00024-X</idno><idno type="PII">S0198-8859(98)00024-X</idno></analytic><monogr><title level="j">Human Immunology</title><title level="j" type="abbrev">HIM</title><idno type="pISSN">0198-8859</idno><idno type="PII">S0198-8859(00)X0041-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">59</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="363">363</biblScope><biblScope unit="page" to="372">372</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Human and nonhuman primates have multiple DR B1 and non-B1 alleles. However, the role of mismatched DR non-B1 alleles in primary alloimmune responses is not well understood. Macaques, which share close DNA homologies with human MHC genes and have a high number of β-chain genes in the DR subregion, are preeminent preclinical models for immunologic studies of transplant tolerance and immunosuppression. In this study, we examined the effect of allogeneic MHC Class II DRB mismatches in Th1- and Th2-like cytokine responses elicited in one-way MLR cultures in rhesus macaques. An ELISPOT method was used to estimate cytokine secretion at the single cell level. Molecular typing for DRB1 and DR non-B1 alleles was performed by a moderate-high resolution PCR-SSP method using a panel of 55 primer pairs covering 74 DRB alleles and clusters. Of 35 unrelated combinations, 66% had multiple (≥2) allelic MM at DRB1 and DR non-B1 with no significant correlation between numbers of DRB1 and DR non-B1 mismatches. Pairs with 1 or 0 MM were assigned to a mono/null MM group to obtain sufficient numbers for statistical analysis. The pairs differing by multiple vs. mono/null DRB1 MM showed no significant difference in cytokine prevalence (P = 0.69). In contrast, high IFN-γ/IL4 SFC ratios were noted in pairs with multiple vs. mono/null DR non-B1 MM (p = 0.0009). IFN-γ/IL-10 spot forming cell (SFC) ratios were consistent with IFN-γ/IL-4 SFC ratios (r = 0.98). Multiple DR non-B1 mismatches showed a trend towards higher MLR proliferative responses, although the stimulation index did not reflect the dominant cytokine response. These observations suggest a bias towards Th1-like cytokine production under allostimulation with multiple DR non-B1 gene products. Further study of the primary structure of DR non-B1 determinants may be helpful in understanding the fine molecular mechanisms governing the regulation of cytokine profiles during allostimulation in primates.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>MLR</term><term>mixed lymphocyte reaction</term></item><item><term>MHC</term><term>major histocompatibility complex</term></item><item><term>NMS</term><term>normal monkey serum</term></item><item><term>SI</term><term>stimulation index</term></item><item><term>RR</term><term>relative response</term></item><item><term>ELISPOT</term><term>enzyme linked immunospot</term></item><item><term>SFC</term><term>spot forming cells</term></item><item><term>MM</term><term>mismatches</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-03-06">Modified</change><change when="1998">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L7WBN221-S/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="GR1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="GR2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="GR3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="GR4"></istex:entity><istex:entity SYSTEM="gr5" NDATA="IMAGE" name="GR5"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>HIM</jid><aid>5256</aid><ce:pii>S0198-8859(98)00024-X</ce:pii><ce:doi>10.1016/S0198-8859(98)00024-X</ce:doi><ce:copyright type="society" year="1998">American Society for Histocompatibility and Immunogenetics</ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>Supported by NIH grants #ROI AII22293 and ROI AI39793.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Original Articles</ce:textfn></ce:dochead><ce:title>DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</ce:title><ce:author-group><ce:author><ce:given-name>A.L.</ce:given-name><ce:surname>Lobashevsky</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.X.</ce:given-name><ce:surname>Wang</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.F.</ce:given-name><ce:surname>George</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.</ce:given-name><ce:surname>Contreras</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.</ce:given-name><ce:surname>Townsend</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.M.</ce:given-name><ce:surname>Thomas</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>jthomas@uab.edu</ce:e-address></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Address reprint requests to: Dr. Judith M. Thomas, UAB Transplant Center, Boshell Diabetes Building 802, 1808 7th Street South, Birmingham, AL 35294-0012</ce:text></ce:correspondence></ce:author-group><ce:date-received day="21" month="1" year="1998"></ce:date-received><ce:date-revised day="6" month="3" year="1998"></ce:date-revised><ce:date-accepted day="9" month="3" year="1998"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Human and nonhuman primates have multiple DR B1 and non-B1 alleles. However, the role of mismatched DR non-B1 alleles in primary alloimmune responses is not well understood. Macaques, which share close DNA homologies with human MHC genes and have a high number of β-chain genes in the DR subregion, are preeminent preclinical models for immunologic studies of transplant tolerance and immunosuppression. In this study, we examined the effect of allogeneic MHC Class II DRB mismatches in Th1- and Th2-like cytokine responses elicited in one-way MLR cultures in rhesus macaques. An ELISPOT method was used to estimate cytokine secretion at the single cell level. Molecular typing for DRB1 and DR non-B1 alleles was performed by a moderate-high resolution PCR-SSP method using a panel of 55 primer pairs covering 74 DRB alleles and clusters. Of 35 unrelated combinations, 66% had multiple (≥2) allelic MM at DRB1 and DR non-B1 with no significant correlation between numbers of DRB1 and DR non-B1 mismatches. Pairs with 1 or 0 MM were assigned to a mono/null MM group to obtain sufficient numbers for statistical analysis. The pairs differing by multiple vs. mono/null DRB1 MM showed no significant difference in cytokine prevalence (<ce:italic>P</ce:italic> = 0.69). In contrast, high IFN-γ/IL4 SFC ratios were noted in pairs with multiple vs. mono/null DR non-B1 MM (<ce:italic>p</ce:italic> = 0.0009). IFN-γ/IL-10 spot forming cell (SFC) ratios were consistent with IFN-γ/IL-4 SFC ratios (<ce:italic>r</ce:italic> = 0.98). Multiple DR non-B1 mismatches showed a trend towards higher MLR proliferative responses, although the stimulation index did not reflect the dominant cytokine response. These observations suggest a bias towards Th1-like cytokine production under allostimulation with multiple DR non-B1 gene products. Further study of the primary structure of DR non-B1 determinants may be helpful in understanding the fine molecular mechanisms governing the regulation of cytokine profiles during allostimulation in primates.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="abr"><ce:section-title>Abbreviations</ce:section-title><ce:keyword><ce:text>MLR</ce:text><ce:keyword><ce:text>mixed lymphocyte reaction</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>MHC</ce:text><ce:keyword><ce:text>major histocompatibility complex</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>NMS</ce:text><ce:keyword><ce:text>normal monkey serum</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>SI</ce:text><ce:keyword><ce:text>stimulation index</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>RR</ce:text><ce:keyword><ce:text>relative response</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>ELISPOT</ce:text><ce:keyword><ce:text>enzyme linked immunospot</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>SFC</ce:text><ce:keyword><ce:text>spot forming cells</ce:text></ce:keyword></ce:keyword><ce:keyword><ce:text>MM</ce:text><ce:keyword><ce:text>mismatches</ce:text></ce:keyword></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>DR Non-B1 Mismatches Influence Allogeneic MLR-Induced TH1- or TH2-Like Cytokine Responses in Rhesus Monkeys</title></titleInfo><name type="personal"><namePart type="given">A.L.</namePart><namePart type="family">Lobashevsky</namePart><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.X.</namePart><namePart type="family">Wang</namePart><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.F.</namePart><namePart type="family">George</namePart><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Contreras</namePart><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Townsend</namePart><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.M.</namePart><namePart type="family">Thomas</namePart><affiliation>Division of Transplantation Immunology, Department of Surgery and Transplant Center, Birmingham, Alabama USA</affiliation><affiliation>Address reprint requests to: Dr. Judith M. Thomas, UAB Transplant Center, Boshell Diabetes Building 802, 1808 7th Street South, Birmingham, AL 35294-0012</affiliation><affiliation>E-mail: jthomas@uab.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued><dateModified encoding="w3cdtf">1998-03-06</dateModified><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Human and nonhuman primates have multiple DR B1 and non-B1 alleles. However, the role of mismatched DR non-B1 alleles in primary alloimmune responses is not well understood. Macaques, which share close DNA homologies with human MHC genes and have a high number of β-chain genes in the DR subregion, are preeminent preclinical models for immunologic studies of transplant tolerance and immunosuppression. In this study, we examined the effect of allogeneic MHC Class II DRB mismatches in Th1- and Th2-like cytokine responses elicited in one-way MLR cultures in rhesus macaques. An ELISPOT method was used to estimate cytokine secretion at the single cell level. Molecular typing for DRB1 and DR non-B1 alleles was performed by a moderate-high resolution PCR-SSP method using a panel of 55 primer pairs covering 74 DRB alleles and clusters. Of 35 unrelated combinations, 66% had multiple (≥2) allelic MM at DRB1 and DR non-B1 with no significant correlation between numbers of DRB1 and DR non-B1 mismatches. Pairs with 1 or 0 MM were assigned to a mono/null MM group to obtain sufficient numbers for statistical analysis. The pairs differing by multiple vs. mono/null DRB1 MM showed no significant difference in cytokine prevalence (P = 0.69). In contrast, high IFN-γ/IL4 SFC ratios were noted in pairs with multiple vs. mono/null DR non-B1 MM (p = 0.0009). IFN-γ/IL-10 spot forming cell (SFC) ratios were consistent with IFN-γ/IL-4 SFC ratios (r = 0.98). Multiple DR non-B1 mismatches showed a trend towards higher MLR proliferative responses, although the stimulation index did not reflect the dominant cytokine response. These observations suggest a bias towards Th1-like cytokine production under allostimulation with multiple DR non-B1 gene products. Further study of the primary structure of DR non-B1 determinants may be helpful in understanding the fine molecular mechanisms governing the regulation of cytokine profiles during allostimulation in primates.</abstract><note>Supported by NIH grants #ROI AII22293 and ROI AI39793.</note><note type="content">Section title: Original Articles</note><note type="content">FIGURE 1: MHC class II typing of representative animal. DRB1∗0309, DRB1∗0403/05, DRB1∗1006, DRB1∗1002/04; DRB3∗0402/05; DRB5∗0301/02/04; DRB6∗0101, DRB6∗0103; DRBw101; DRBw201; DRBw701. PCR products were size separated on 2% agarose gel containing 0.5 μg/ml of ethidium bromide. The entire medium/high resolution-typing panel consisted of 55 allele specific primer mixtures. The name of the amplified allele(s) is given above each lane giving positive signal. The arrows indicate the migration of the 430-bp globin internal positive control and allele specific PCR products varying from 120 to 250 bp.</note><note type="content">FIGURE 2: Distribution of DRB1 and DR non-B1 mismatches in random unrelated responder/stimulator combinations. The animals were DNA typed for DRB locus using PCR-SSP. Groupings were based on the numbers of mismatched DRB alleles. Open sectors correspond to donor/recipient combinations with 0 DRB MM; black sectors correspond to donor/recipient combinations with 1 DRB MM; hatched sectors correspond to donor/recipient combinations with multiple (2–6) DRB MM. The numbers of unrelated combinations of responder/stimulator are: for DRB1 alleles multiple mismatches—23, 1 mismatch—11, 0 mismatches—1; for DR non B1 alleles, multiple mismatches—10, 1 mismatch—3, 0 mismatches—2.</note><note type="content">FIGURE 3: Influence of DR non-B1 incompatibilities on Th1/Th2-like response. Responder T cells were allostimulated with irradiated donor PBMC differing by various numbers of DRB1 and DR non-B1 specificities.</note><note type="content">FIGURE 4: Influence of multiple DR non-B1 MM on T cell alloproliferative responses. The results, which represent the mean value of triplicates, were expressed by the stimulation index (SI) or relative response (RR).</note><note type="content">FIGURE 5: Kinetics of IFN-γ production in serum of kidney recipients which were transplanted with organs differing by various numbers of DR non-B1 MM. One animal was 6 DR non-B1 MM with the donor, 2 animals were 3 DR non-B1 MM with their donors and one animal was 0 DR non-B1 MM with the donor. Monkey serum samples were tested on 3, 4 and 14 days after surgery using ELISA.</note><subject lang="en"><genre>Abbreviations</genre><topic>MLR : mixed lymphocyte reaction</topic><topic>MHC : major histocompatibility complex</topic><topic>NMS : normal monkey serum</topic><topic>SI : stimulation index</topic><topic>RR : relative response</topic><topic>ELISPOT : enzyme linked immunospot</topic><topic>SFC : spot forming cells</topic><topic>MM : mismatches</topic></subject><relatedItem type="host"><titleInfo><title>Human Immunology</title></titleInfo><titleInfo type="abbreviated"><title>HIM</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued></originInfo><identifier type="ISSN">0198-8859</identifier><identifier type="PII">S0198-8859(00)X0041-9</identifier><part><date>1998</date><detail type="volume"><number>59</number><caption>vol.</caption></detail><detail type="issue"><number>6</number><caption>no.</caption></detail><extent unit="issue-pages"><start>325</start><end>386</end></extent><extent unit="pages"><start>363</start><end>372</end></extent></part></relatedItem><identifier type="istex">DA4A6943CC5129B5ED61A11C7AACFFF93A2C008C</identifier><identifier type="ark">ark:/67375/6H6-L7WBN221-S</identifier><identifier type="DOI">10.1016/S0198-8859(98)00024-X</identifier><identifier type="PII">S0198-8859(98)00024-X</identifier><accessCondition type="use and reproduction" contentType="copyright">©1998 American Society for Histocompatibility and Immunogenetics</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>American Society for Histocompatibility and Immunogenetics, ©1998</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-L7WBN221-S/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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