| First Author | Zheng B | Year | 2007 |
| Journal | Clin Exp Immunol | Volume | 149 |
| Issue | 3 | Pages | 579-85 |
| PubMed ID | 17590174 | Mgi Jnum | J:123552 |
| Mgi Id | MGI:3718820 | Doi | 10.1111/j.1365-2249.2007.03440.x |
| Citation | Zheng B, et al. (2007) IgM plays an important role in induction of collagen-induced arthritis. Clin Exp Immunol 149(3):579-85 |
| abstractText | IgM is one major type of B cell receptor (BCR) expressed on most of the B cells from immature to mature stages. During normal B cell ontogeny, signals transduced through the IgM BCR play an important role in regulating B cell maturation and survival at multiple checkpoints. In addition, IgM BCR is also required for antigen-dependent differentiation and activation of B cells. However, whether IgM BCR-mediated signalling is important for the pathogenesis of autoimmune diseases remains elusive. Using IgM-deficient mice, we examined the effect of absence of IgM on the development of collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis (RA). Compared to their wild-type littermates, IgM-deficient mice were either resistant to arthritis induction or developed significantly less severe arthritis. There was a significant decrease of autoantibody production in IgM-deficient mice, particularly IgG2a antibodies, which is believed to be pathogenic in CIA. Thus, although IgM(-/-) mice have relatively normal B cell development with IgD BCR replacing IgM BCR, the absence of IgM-mediated signals has a profound impact on the development of CIA, indicating that IgM plays an important role in the development and pathogenesis of autoimmune arthritis and IgM-mediated signalling is critical in the generation of pathogenic autoreactive antibodies. |
