| First Author | Taneja V | Year | 2007 |
| Journal | Mol Immunol | Volume | 44 |
| Issue | 11 | Pages | 2988-96 |
| PubMed ID | 17303243 | Mgi Jnum | J:119712 |
| Mgi Id | MGI:3703178 | Doi | 10.1016/j.molimm.2006.12.026 |
| Citation | Taneja V, et al. (2007) B cells are important as antigen presenting cells for induction of MHC-restricted arthritis in transgenic mice. Mol Immunol 44(11):2988-96 |
| abstractText | Rheumatoid arthritis and its animal model, collagen-induced arthritis, are known as a T and B cell dependent disease. To analyze the role of B cells in arthritis, we generated B cell deficient (muMT) mice carrying HLA-DQ8 as transgene, Abetao.DQ8.mumt mice. HLA-DQ8 transgenic mice (Abetao.DQ8) are susceptible to collagen induced arthritis, an animal model for inflammatory arthritis. Deletion of IgM gene led to the absence of B cells while T cells were comparable to Abetao.DQ8 mice. Arthritis and autoantibodies was completely abrogated in B cell deficient DQ8 mice. T cell response and proinflammatory cytokine production in response to type II collagen and its derived peptides in vitro was significantly decreased despite an increased number of Mac-1 positive cells in DQ8.mumt mice compared to DQ8 mice suggesting B cells could be important for antigen presentation as well. In vitro substitution of B cells from wild type mice restored the response in DQ8.mumt mice. B cells could also present CII-derived peptides to antigen-specific DQ8-restricted hybridomas reinforcing the role of B cells in presentation of antigens to T cells. The data suggest that B cells can be involved in pathogenesis of arthritis by producing autoantibodies and antigen presentation. |
