Source:http://linkedlifedata.com/resource/pubmed/id/12023391
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2002-5-22
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pubmed:abstractText |
To investigate the role of CD4 and CD8 T cells in arthritis, we generated transgenic mice deficient in CD4 and CD8 molecules expressing RA-susceptible gene HLA-DQ8. DQ8.CD4(-/-) mice were resistant to developing collagen-induced arthritis (CIA). However, DQ8.CD8(-/-) mice developed CIA with increased incidence and more severity than DQ8 mice. Both DQ8.CD8(-/-) and DQ8 mice produced rheumatoid factor. In addition, DQ8.CD8(-/-) mice produced antinuclear Abs. The B cell compartment and expression of DQ8 were normal in all the strains, although frequency of cells expressing DQ8 was less in CD4(-/-) mice. An increased frequency of CD3(+) double-negative (DN) T cells was found in DQ8.CD8(-/-) compared with DQ8.CD4(-/-) and DQ8 mice. These CD3(+) DN T cells produced high amounts of IL-10 in CD8-deficient mice. Analysis of cell division using a cell cycle tracking dye showed a higher rate of division of CD3(+) and CD3(+) DN T cells in DQ8.CD8(-/-) mice compared with DQ8.CD4(-/-) and DQ8 mice. Decreased apoptosis was seen in CIA-susceptible DQ8 and CD8-deficient mice, indicating a defect in activation-induced cell death. These observations suggest that CD4 cells are necessary for initiation of CIA in DQ8 mice. We hypothesize that CD8(+) T cells are not capable of initiating CIA in DQ8-transgenic mice but may have a regulatory/protective effect.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Antinuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DQ Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DQ8 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Rheumatoid Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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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 |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5867-75
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12023391-Animals,
pubmed-meshheading:12023391-Antibodies, Antinuclear,
pubmed-meshheading:12023391-Arthritis, Rheumatoid,
pubmed-meshheading:12023391-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12023391-CD8-Positive T-Lymphocytes,
pubmed-meshheading:12023391-Collagen,
pubmed-meshheading:12023391-Disease Susceptibility,
pubmed-meshheading:12023391-Female,
pubmed-meshheading:12023391-HLA-DQ Antigens,
pubmed-meshheading:12023391-Interferon-gamma,
pubmed-meshheading:12023391-Lymphocyte Activation,
pubmed-meshheading:12023391-Male,
pubmed-meshheading:12023391-Mice,
pubmed-meshheading:12023391-Mice, Transgenic,
pubmed-meshheading:12023391-Rheumatoid Factor,
pubmed-meshheading:12023391-Tumor Necrosis Factor-alpha
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pubmed:year |
2002
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pubmed:articleTitle |
CD4 and CD8 T cells in susceptibility/protection to collagen-induced arthritis in HLA-DQ8-transgenic mice: implications for rheumatoid arthritis.
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pubmed:affiliation |
Department of Immunology and Division of Rheumatology, Mayo Clinic, Rochester, MN 55905, USA. taneja.veena@mayo.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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