Differential Role of B Cells and IL-17 Versus IFN-γ During Early and Late Rejection of Pig Islet Xenografts in Mice.
Identifieur interne : 000873 ( Main/Exploration ); précédent : 000872; suivant : 000874Differential Role of B Cells and IL-17 Versus IFN-γ During Early and Late Rejection of Pig Islet Xenografts in Mice.
Auteurs : Hee Kap Kang [États-Unis] ; Shusen Wang ; Anil Dangi ; Xiaomin Zhang ; Amar Singh ; Lei Zhang ; James M. Rosati ; Wilma Suarez-Pinzon ; Xuelian Deng ; Xiaoyan Chen ; Edward B. Thorp ; Bernhard J. Hering ; Stephen D. Miller ; Xunrong LuoSource :
- Transplantation [ 1534-6080 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Facteurs temps (MeSH), Hétérogreffes (MeSH), Interféron gamma (biosynthèse), Interleukine-17 (biosynthèse), Lymphocytes B (immunologie), Modèles animaux de maladie humaine (MeSH), Mâle (MeSH), Rejet du greffon (anatomopathologie), Rejet du greffon (immunologie), Rejet du greffon (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Survie du greffon (immunologie), Test ELISA (MeSH), Tolérance immunitaire (MeSH), Transplantation d'ilots de Langerhans (immunologie).
- MESH :
- anatomopathologie : Rejet du greffon.
- biosynthèse : Interféron gamma, Interleukine-17.
- immunologie : Lymphocytes B, Rejet du greffon, Survie du greffon, Transplantation d'ilots de Langerhans.
- métabolisme : Rejet du greffon.
- Animaux, Facteurs temps, Hétérogreffes, Modèles animaux de maladie humaine, Mâle, Souris, Souris de lignée C57BL, Test ELISA, Tolérance immunitaire.
English descriptors
- KwdEn :
- Animals (MeSH), B-Lymphocytes (immunology), Disease Models, Animal (MeSH), Enzyme-Linked Immunosorbent Assay (MeSH), Graft Rejection (immunology), Graft Rejection (metabolism), Graft Rejection (pathology), Graft Survival (immunology), Heterografts (MeSH), Immune Tolerance (MeSH), Interferon-gamma (biosynthesis), Interleukin-17 (biosynthesis), Islets of Langerhans Transplantation (immunology), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Time Factors (MeSH).
- MESH :
- chemical , biosynthesis : Interferon-gamma, Interleukin-17.
- immunology : B-Lymphocytes, Graft Rejection, Graft Survival, Islets of Langerhans Transplantation.
- metabolism : Graft Rejection.
- pathology : Graft Rejection.
- Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Heterografts, Immune Tolerance, Male, Mice, Mice, Inbred C57BL, Time Factors.
Abstract
BACKGROUND
Xenogeneic islet transplantation is an emerging therapeutic option for diabetic patients. However, immunological tolerance to xenogeneic islets remains a challenge.
METHODS
The current study used a pig-to-mouse discordant xenogeneic islet transplant model to examine antidonor xenogeneic immune responses during early and late rejection and to determine experimental therapeutic interventions that promote durable pig islet xenograft survival.
RESULTS
We found that during early acute rejection of pig islet xenografts, the rejecting hosts exhibited a heavy graft infiltration with B220 B cells and a robust antipig antibody production. In addition, early donor-stimulated IL-17 production, but not IFN-γ production, dominated during early acute rejection. Recipient treatment with donor apoptotic 1-ethyl-3-(3'-dimethylaminopropyl)-carbodiimide-treated splenocytes significantly inhibited antidonor IL-17 response, and when combined with B cell depletion and a short course of rapamycin led to survival of pig islet xenografts beyond 100 days in approximately 65% recipients. Interestingly, treated recipients in this model experienced late rejection between 100 and 200 days posttransplant, which coincided with B cell reconstitution and an ensuing emergence of a robust antidonor IFN-γ, but not IL-17, response.
CONCLUSIONS
These findings reveal that early and late rejection of pig islet xenografts may be dominated by different immune responses and that maintenance of long-term xenogeneic tolerance will require strategies that target the temporal sequence of antixenogeneic immune responses.
DOI: 10.1097/TP.0000000000001489
PubMed: 27893617
PubMed Central: PMC5441974
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Rosati</name></author><author><name sortKey="Suarez Pinzon, Wilma" sort="Suarez Pinzon, Wilma" uniqKey="Suarez Pinzon W" first="Wilma" last="Suarez-Pinzon">Wilma Suarez-Pinzon</name></author><author><name sortKey="Deng, Xuelian" sort="Deng, Xuelian" uniqKey="Deng X" first="Xuelian" last="Deng">Xuelian Deng</name></author><author><name sortKey="Chen, Xiaoyan" sort="Chen, Xiaoyan" uniqKey="Chen X" first="Xiaoyan" last="Chen">Xiaoyan Chen</name></author><author><name sortKey="Thorp, Edward B" sort="Thorp, Edward B" uniqKey="Thorp E" first="Edward B" last="Thorp">Edward B. Thorp</name></author><author><name sortKey="Hering, Bernhard J" sort="Hering, Bernhard J" uniqKey="Hering B" first="Bernhard J" last="Hering">Bernhard J. Hering</name></author><author><name sortKey="Miller, Stephen D" sort="Miller, Stephen D" uniqKey="Miller S" first="Stephen D" last="Miller">Stephen D. Miller</name></author><author><name sortKey="Luo, Xunrong" sort="Luo, Xunrong" uniqKey="Luo X" first="Xunrong" last="Luo">Xunrong Luo</name></author></analytic><series><title level="j">Transplantation</title><idno type="eISSN">1534-6080</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>B-Lymphocytes (immunology)</term><term>Disease Models, Animal (MeSH)</term><term>Enzyme-Linked Immunosorbent Assay (MeSH)</term><term>Graft Rejection (immunology)</term><term>Graft Rejection (metabolism)</term><term>Graft Rejection (pathology)</term><term>Graft Survival (immunology)</term><term>Heterografts (MeSH)</term><term>Immune Tolerance (MeSH)</term><term>Interferon-gamma (biosynthesis)</term><term>Interleukin-17 (biosynthesis)</term><term>Islets of Langerhans Transplantation (immunology)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Time Factors (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Facteurs temps (MeSH)</term><term>Hétérogreffes (MeSH)</term><term>Interféron gamma (biosynthèse)</term><term>Interleukine-17 (biosynthèse)</term><term>Lymphocytes B (immunologie)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Mâle (MeSH)</term><term>Rejet du greffon (anatomopathologie)</term><term>Rejet du greffon (immunologie)</term><term>Rejet du greffon (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Survie du greffon (immunologie)</term><term>Test ELISA (MeSH)</term><term>Tolérance immunitaire (MeSH)</term><term>Transplantation d'ilots de Langerhans (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon-gamma</term><term>Interleukin-17</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Rejet du greffon</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron gamma</term><term>Interleukine-17</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes B</term><term>Rejet du greffon</term><term>Survie du greffon</term><term>Transplantation d'ilots de Langerhans</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>B-Lymphocytes</term><term>Graft Rejection</term><term>Graft Survival</term><term>Islets of Langerhans Transplantation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Graft Rejection</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Rejet du greffon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Graft Rejection</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Heterografts</term><term>Immune Tolerance</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Facteurs temps</term><term>Hétérogreffes</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Test ELISA</term><term>Tolérance immunitaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Xenogeneic islet transplantation is an emerging therapeutic option for diabetic patients. However, immunological tolerance to xenogeneic islets remains a challenge.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>The current study used a pig-to-mouse discordant xenogeneic islet transplant model to examine antidonor xenogeneic immune responses during early and late rejection and to determine experimental therapeutic interventions that promote durable pig islet xenograft survival.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>We found that during early acute rejection of pig islet xenografts, the rejecting hosts exhibited a heavy graft infiltration with B220 B cells and a robust antipig antibody production. In addition, early donor-stimulated IL-17 production, but not IFN-γ production, dominated during early acute rejection. Recipient treatment with donor apoptotic 1-ethyl-3-(3'-dimethylaminopropyl)-carbodiimide-treated splenocytes significantly inhibited antidonor IL-17 response, and when combined with B cell depletion and a short course of rapamycin led to survival of pig islet xenografts beyond 100 days in approximately 65% recipients. Interestingly, treated recipients in this model experienced late rejection between 100 and 200 days posttransplant, which coincided with B cell reconstitution and an ensuing emergence of a robust antidonor IFN-γ, but not IL-17, response.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>These findings reveal that early and late rejection of pig islet xenografts may be dominated by different immune responses and that maintenance of long-term xenogeneic tolerance will require strategies that target the temporal sequence of antixenogeneic immune responses.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27893617</PMID><DateCompleted><Year>2017</Year><Month>09</Month><Day>13</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1534-6080</ISSN><JournalIssue CitedMedium="Internet"><Volume>101</Volume><Issue>8</Issue><PubDate><Year>2017</Year><Month>08</Month></PubDate></JournalIssue><Title>Transplantation</Title><ISOAbbreviation>Transplantation</ISOAbbreviation></Journal><ArticleTitle>Differential Role of B Cells and IL-17 Versus IFN-γ During Early and Late Rejection of Pig Islet Xenografts in Mice.</ArticleTitle><Pagination><MedlinePgn>1801-1810</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/TP.0000000000001489</ELocationID><Abstract><AbstractText Label="BACKGROUND">Xenogeneic islet transplantation is an emerging therapeutic option for diabetic patients. However, immunological tolerance to xenogeneic islets remains a challenge.</AbstractText><AbstractText Label="METHODS">The current study used a pig-to-mouse discordant xenogeneic islet transplant model to examine antidonor xenogeneic immune responses during early and late rejection and to determine experimental therapeutic interventions that promote durable pig islet xenograft survival.</AbstractText><AbstractText Label="RESULTS">We found that during early acute rejection of pig islet xenografts, the rejecting hosts exhibited a heavy graft infiltration with B220 B cells and a robust antipig antibody production. In addition, early donor-stimulated IL-17 production, but not IFN-γ production, dominated during early acute rejection. Recipient treatment with donor apoptotic 1-ethyl-3-(3'-dimethylaminopropyl)-carbodiimide-treated splenocytes significantly inhibited antidonor IL-17 response, and when combined with B cell depletion and a short course of rapamycin led to survival of pig islet xenografts beyond 100 days in approximately 65% recipients. Interestingly, treated recipients in this model experienced late rejection between 100 and 200 days posttransplant, which coincided with B cell reconstitution and an ensuing emergence of a robust antidonor IFN-γ, but not IL-17, response.</AbstractText><AbstractText Label="CONCLUSIONS">These findings reveal that early and late rejection of pig islet xenografts may be dominated by different immune responses and that maintenance of long-term xenogeneic tolerance will require strategies that target the temporal sequence of antixenogeneic immune responses.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Hee Kap</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>1 Division of Nephrology and Hypertension, Northwestern University Feinberg School of Medicine, Chicago, IL. 2 Tianjin Union Medical Center, Nankai University Affiliated Hospital, Tianjin, China. 3 Comprehensive Transplant Center, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL. 4 Department of Surgery, University of Minnesota, Schulze Diabetes Institute, Minneapolis, MN. 5 Division of Endocrinology, First Affiliated Hospital of Guangzhou Medical University, Guangdong, China. 6 Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL. 7 Department of Microbiology and Immunology, Interdepartmental Immunobiology Center, Northwestern University Feinberg School of Medicine, Chicago, IL.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Shusen</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Dangi</LastName><ForeName>Anil</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiaomin</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Singh</LastName><ForeName>Amar</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Lei</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Rosati</LastName><ForeName>James M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Suarez-Pinzon</LastName><ForeName>Wilma</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Xuelian</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Thorp</LastName><ForeName>Edward B</ForeName><Initials>EB</Initials></Author><Author ValidYN="Y"><LastName>Hering</LastName><ForeName>Bernhard J</ForeName><Initials>BJ</Initials></Author><Author ValidYN="Y"><LastName>Miller</LastName><ForeName>Stephen D</ForeName><Initials>SD</Initials></Author><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Xunrong</ForeName><Initials>X</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>DP2 DK083099</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS026543</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL122309</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA060553</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 AI102463</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Transplantation</MedlineTA><NlmUniqueID>0132144</NlmUniqueID><ISSNLinking>0041-1337</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020381">Interleukin-17</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001402" MajorTopicYN="N">B-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004797" MajorTopicYN="N">Enzyme-Linked Immunosorbent Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006084" MajorTopicYN="N">Graft Rejection</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006085" MajorTopicYN="N">Graft Survival</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D064593" MajorTopicYN="N">Heterografts</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007108" MajorTopicYN="Y">Immune Tolerance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020381" MajorTopicYN="N">Interleukin-17</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016381" MajorTopicYN="N">Islets of Langerhans Transplantation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Hering</name><name sortKey="Luo, Xunrong" sort="Luo, Xunrong" uniqKey="Luo X" first="Xunrong" last="Luo">Xunrong Luo</name><name sortKey="Miller, Stephen D" sort="Miller, Stephen D" uniqKey="Miller S" first="Stephen D" last="Miller">Stephen D. Miller</name><name sortKey="Rosati, James M" sort="Rosati, James M" uniqKey="Rosati J" first="James M" last="Rosati">James M. Rosati</name><name sortKey="Singh, Amar" sort="Singh, Amar" uniqKey="Singh A" first="Amar" last="Singh">Amar Singh</name><name sortKey="Suarez Pinzon, Wilma" sort="Suarez Pinzon, Wilma" uniqKey="Suarez Pinzon W" first="Wilma" last="Suarez-Pinzon">Wilma Suarez-Pinzon</name><name sortKey="Thorp, Edward B" sort="Thorp, Edward B" uniqKey="Thorp E" first="Edward B" last="Thorp">Edward B. Thorp</name><name sortKey="Wang, Shusen" sort="Wang, Shusen" uniqKey="Wang S" first="Shusen" last="Wang">Shusen Wang</name><name sortKey="Zhang, Lei" sort="Zhang, Lei" uniqKey="Zhang L" first="Lei" last="Zhang">Lei Zhang</name><name sortKey="Zhang, Xiaomin" sort="Zhang, Xiaomin" uniqKey="Zhang X" first="Xiaomin" last="Zhang">Xiaomin Zhang</name></noCountry><country name="États-Unis"><region name="Illinois"><name sortKey="Kang, Hee Kap" sort="Kang, Hee Kap" uniqKey="Kang H" first="Hee Kap" last="Kang">Hee Kap Kang</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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