Differential regulation of in vitro humoral and cellular immune responsiveness in Brugia pahangi-infected jirds.
Identifieur interne : 006100 ( PubMed/Corpus ); précédent : 006099; suivant : 006101Differential regulation of in vitro humoral and cellular immune responsiveness in Brugia pahangi-infected jirds.
Auteurs : R C Prier ; P J LammieSource :
- Infection and immunity [ 0019-9567 ] ; 1988.
English descriptors
- KwdEn :
- Animals, Antibodies, Helminth (biosynthesis), Antibody Formation, Brugia, Cells, Cultured, Dose-Response Relationship, Immunologic, Elephantiasis, Filarial (immunology), Filariasis (immunology), Gerbillinae (immunology), Immunization, In Vitro Techniques, Lymph Nodes (immunology), Lymphocyte Activation, Spleen (immunology).
- MESH :
- chemical , biosynthesis : Antibodies, Helminth.
- immunology : Elephantiasis, Filarial, Filariasis, Gerbillinae, Lymph Nodes, Spleen.
- Animals, Antibody Formation, Brugia, Cells, Cultured, Dose-Response Relationship, Immunologic, Immunization, In Vitro Techniques, Lymphocyte Activation.
Abstract
Patent filarial infection is associated with the downregulation of parasite-specific immune reactivity. In the present study, the relationship between in vitro parasite antigen-specific humoral and cellular immune responsiveness was investigated in Brugia pahangi-infected jirds and in jirds immunized with soluble antigens. Spleen cells from B. pahangi-immunized jirds or from jirds with prepatent infections mounted significant in vitro proliferative and antibody responses to B. pahangi. The antigen concentration which elicited optimal antibody production was 10- to 10,000-fold lower than that required to stimulate optimal blastogenesis. Lymph node cells from both immunized and infected jirds consistently produced lower levels of parasite-specific antibody than spleen cells, yet generated higher proliferative responses to filarial antigen. A dissociation between in vitro antibody production and proliferation was also observed in experiments with spleen cells from microfilaremic jirds; spleen cells from patent animals did not proliferate when stimulated with B. pahangi antigen, but did produce significant levels of parasite-specific antibody. Depletion of adherent or histamine receptor-bearing cells restored the proliferative reactivity of spleen cells from microfilaremic jirds, but had limited effects on antibody production. In admixture experiments, spleen cells from microfilaremic animals suppressed the proliferative responsiveness of cells from keyhole limpet hemocyanin (KLH)-immunized jirds to KLH by 38%, but had no effect on KLH-specific antibody production. The present results support the hypothesis that parasite-specific cellular and humoral reactivity are differentially regulated in experimental filariasis.
PubMed: 3182070
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Differential regulation of in vitro humoral and cellular immune responsiveness in Brugia pahangi-infected jirds.</title><author><name sortKey="Prier, R C" sort="Prier, R C" uniqKey="Prier R" first="R C" last="Prier">R C Prier</name><affiliation><nlm:affiliation>Department of Microbiology, Immunology and Parasitology, Louisiana State University Medical Center, New Orleans 70112.</nlm:affiliation></affiliation></author><author><name sortKey="Lammie, P J" sort="Lammie, P J" uniqKey="Lammie P" first="P J" last="Lammie">P J Lammie</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1988">1988</date><idno type="RBID">pubmed:3182070</idno><idno type="pmid">3182070</idno><idno type="wicri:Area/PubMed/Corpus">006100</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">006100</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differential regulation of in vitro humoral and cellular immune responsiveness in Brugia pahangi-infected jirds.</title><author><name sortKey="Prier, R C" sort="Prier, R C" uniqKey="Prier R" first="R C" last="Prier">R C Prier</name><affiliation><nlm:affiliation>Department of Microbiology, Immunology and Parasitology, Louisiana State University Medical Center, New Orleans 70112.</nlm:affiliation></affiliation></author><author><name sortKey="Lammie, P J" sort="Lammie, P J" uniqKey="Lammie P" first="P J" last="Lammie">P J Lammie</name></author></analytic><series><title level="j">Infection and immunity</title><idno type="ISSN">0019-9567</idno><imprint><date when="1988" type="published">1988</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Helminth (biosynthesis)</term><term>Antibody Formation</term><term>Brugia</term><term>Cells, Cultured</term><term>Dose-Response Relationship, Immunologic</term><term>Elephantiasis, Filarial (immunology)</term><term>Filariasis (immunology)</term><term>Gerbillinae (immunology)</term><term>Immunization</term><term>In Vitro Techniques</term><term>Lymph Nodes (immunology)</term><term>Lymphocyte Activation</term><term>Spleen (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Antibodies, Helminth</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Elephantiasis, Filarial</term><term>Filariasis</term><term>Gerbillinae</term><term>Lymph Nodes</term><term>Spleen</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Antibody Formation</term><term>Brugia</term><term>Cells, Cultured</term><term>Dose-Response Relationship, Immunologic</term><term>Immunization</term><term>In Vitro Techniques</term><term>Lymphocyte Activation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Patent filarial infection is associated with the downregulation of parasite-specific immune reactivity. In the present study, the relationship between in vitro parasite antigen-specific humoral and cellular immune responsiveness was investigated in Brugia pahangi-infected jirds and in jirds immunized with soluble antigens. Spleen cells from B. pahangi-immunized jirds or from jirds with prepatent infections mounted significant in vitro proliferative and antibody responses to B. pahangi. The antigen concentration which elicited optimal antibody production was 10- to 10,000-fold lower than that required to stimulate optimal blastogenesis. Lymph node cells from both immunized and infected jirds consistently produced lower levels of parasite-specific antibody than spleen cells, yet generated higher proliferative responses to filarial antigen. A dissociation between in vitro antibody production and proliferation was also observed in experiments with spleen cells from microfilaremic jirds; spleen cells from patent animals did not proliferate when stimulated with B. pahangi antigen, but did produce significant levels of parasite-specific antibody. Depletion of adherent or histamine receptor-bearing cells restored the proliferative reactivity of spleen cells from microfilaremic jirds, but had limited effects on antibody production. In admixture experiments, spleen cells from microfilaremic animals suppressed the proliferative responsiveness of cells from keyhole limpet hemocyanin (KLH)-immunized jirds to KLH by 38%, but had no effect on KLH-specific antibody production. The present results support the hypothesis that parasite-specific cellular and humoral reactivity are differentially regulated in experimental filariasis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">3182070</PMID><DateCreated><Year>1988</Year><Month>12</Month><Day>20</Day></DateCreated><DateCompleted><Year>1988</Year><Month>12</Month><Day>20</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0019-9567</ISSN><JournalIssue CitedMedium="Print"><Volume>56</Volume><Issue>12</Issue><PubDate><Year>1988</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Differential regulation of in vitro humoral and cellular immune responsiveness in Brugia pahangi-infected jirds.</ArticleTitle><Pagination><MedlinePgn>3052-7</MedlinePgn></Pagination><Abstract><AbstractText>Patent filarial infection is associated with the downregulation of parasite-specific immune reactivity. In the present study, the relationship between in vitro parasite antigen-specific humoral and cellular immune responsiveness was investigated in Brugia pahangi-infected jirds and in jirds immunized with soluble antigens. Spleen cells from B. pahangi-immunized jirds or from jirds with prepatent infections mounted significant in vitro proliferative and antibody responses to B. pahangi. The antigen concentration which elicited optimal antibody production was 10- to 10,000-fold lower than that required to stimulate optimal blastogenesis. Lymph node cells from both immunized and infected jirds consistently produced lower levels of parasite-specific antibody than spleen cells, yet generated higher proliferative responses to filarial antigen. A dissociation between in vitro antibody production and proliferation was also observed in experiments with spleen cells from microfilaremic jirds; spleen cells from patent animals did not proliferate when stimulated with B. pahangi antigen, but did produce significant levels of parasite-specific antibody. Depletion of adherent or histamine receptor-bearing cells restored the proliferative reactivity of spleen cells from microfilaremic jirds, but had limited effects on antibody production. In admixture experiments, spleen cells from microfilaremic animals suppressed the proliferative responsiveness of cells from keyhole limpet hemocyanin (KLH)-immunized jirds to KLH by 38%, but had no effect on KLH-specific antibody production. The present results support the hypothesis that parasite-specific cellular and humoral reactivity are differentially regulated in experimental filariasis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Prier</LastName><ForeName>R C</ForeName><Initials>RC</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Immunology and Parasitology, Louisiana State University Medical Center, New Orleans 70112.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lammie</LastName><ForeName>P J</ForeName><Initials>PJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI-24459</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000909">Antibodies, Helminth</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Parasitol. 1970 Oct;56(5):969-73</RefSource><PMID Version="1">5504534</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1972 Sep;69(9):2701-5</RefSource><PMID Version="1">4403565</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 1973 Jun;52(6):1349-61</RefSource><PMID Version="1">4145025</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Parasitol. 1976 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Version="1">2453554</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000909" MajorTopicYN="N">Antibodies, Helminth</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000917" MajorTopicYN="Y">Antibody Formation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002009" MajorTopicYN="N">Brugia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004306" MajorTopicYN="N">Dose-Response Relationship, Immunologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005368" MajorTopicYN="N">Filariasis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005849" MajorTopicYN="N">Gerbillinae</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007114" MajorTopicYN="N">Immunization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008198" MajorTopicYN="N">Lymph Nodes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008213" MajorTopicYN="Y">Lymphocyte Activation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName><QualifierName 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