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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0026809,
umls-concept:C0032214,
umls-concept:C0035820,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0205390,
umls-concept:C0851285,
umls-concept:C0971858,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1704686,
umls-concept:C1706438,
umls-concept:C2004454,
umls-concept:C2698600
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pubmed:issue |
11
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pubmed:dateCreated |
1996-8-8
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pubmed:abstractText |
Collagen-induced arthritis (CIA) is an experimental autoimmune disease induced by immunization with collagen type II (CII). We studied CIA in CD4- or CD8-deficient DBA/1 mice to further define the roles of CD4+ and CD8+ T cells in the disease. CD4-deficient mice developed severe arthritis, and no differences in incidence, clinical course, and severity were observed between CD4 -/- and CD4 +/- mice. Proliferative responses of lymph node T cells to CII was, however, reduced in CD4 -/- mice, and inflamed joints revealed relative accumulation of CD4-CD8-TCR(alpha)(beta)+ cells. A CII-specific T cell line generated from CD4-deficient mice responded to CII in a MHC-restricted fashion and had a CD4-CD8-TCR(alpha)(beta)+ phenotype. Disease incidence in CD8 -/- mice was significantly decreased compared with CD8 +/- mice, even though the severity of arthritis in arthritic mice was not different. These results suggests a role for CD8+ T cells in initiating CIA. Interestingly, CD8-deficient mice were more susceptible to a second induction of arthritis after remission of initial disease, pointing towards an immunoregulatory role for CD8+ T cells. CD8-deficient mice did not, however, show any defect in oral tolerance induction using CII. Taken together, our findings demonstrate that CD4-CD8-TCR(alpha)(beta) cells can trigger systemic arthritis in CD4-deficient mice and that CD8+ T cells can play dual and opposing roles, important both in initiation of CIA and in providing resistance to reinduction of CIA after recovery from initial disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
156
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4520-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8666829-Animals,
pubmed-meshheading:8666829-Antigens, CD4,
pubmed-meshheading:8666829-Antigens, CD8,
pubmed-meshheading:8666829-Arthritis,
pubmed-meshheading:8666829-Autoantibodies,
pubmed-meshheading:8666829-Autoimmune Diseases,
pubmed-meshheading:8666829-CD8-Positive T-Lymphocytes,
pubmed-meshheading:8666829-Cell Line,
pubmed-meshheading:8666829-Collagen,
pubmed-meshheading:8666829-Immune Tolerance,
pubmed-meshheading:8666829-Lymphocyte Activation,
pubmed-meshheading:8666829-Mice,
pubmed-meshheading:8666829-Mice, Inbred DBA,
pubmed-meshheading:8666829-Mice, Mutant Strains,
pubmed-meshheading:8666829-T-Lymphocyte Subsets,
pubmed-meshheading:8666829-Time Factors
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pubmed:year |
1996
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pubmed:articleTitle |
Collagen-induced arthritis in CD4- or CD8-deficient mice: CD8+ T cells play a role in initiation and regulate recovery phase of collagen-induced arthritis.
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pubmed:affiliation |
Amgen Institute, Ontario Cancer Institute, Ontario, Canada.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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