| First Author | Svensson L | Year | 1998 |
| Journal | Clin Exp Immunol | Volume | 111 |
| Issue | 3 | Pages | 521-6 |
| PubMed ID | 9528892 | Mgi Jnum | J:46988 |
| Mgi Id | MGI:1202468 | Doi | 10.1046/j.1365-2249.1998.00529.x |
| Citation | Svensson L, et al. (1998) B cell-deficient mice do not develop type II collagen-induced arthritis (CIA). Clin Exp Immunol 111(3):521-6 |
| abstractText | To investigate the role of B cells in the development of CIA, a model for rheumatoid arthritis, we investigated susceptibility to CIA in mice lacking B cells due to the deletion of the IgM heavy chain gene (muMT). The muMT deletion was backcrossed into two different CIA-susceptible strains, B10.Q and B10.RIII. Two different variants of the CIA model are inducible in these strains: in B10.Q with rat type II collagen (CII) and in B10.RIII with bovine CII. Homozygous deletion of the IgM gene led to the absence of B cells and dramatically reduced immunoglobulin levels compared with wild-type mice. The deletion of IgM totally abrogated development of CIA in both strains, although the anti- CII T cell response did not differ between the muMT and wild-type controls. We conclude that B cells play a crucial role in the development of CIA. |
