| First Author | Gross JA | Year | 2001 |
| Journal | Immunity | Volume | 15 |
| Issue | 2 | Pages | 289-302 |
| PubMed ID | 11520463 | Mgi Jnum | J:71301 |
| Mgi Id | MGI:2149528 | Doi | 10.1016/s1074-7613(01)00183-2 |
| Citation | Gross JA, et al. (2001) TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease. impaired B cell maturation in mice lacking BLyS. Immunity 15(2):289-302 |
| abstractText | BLyS and APRIL have similar but distinct biological roles, mediated through two known TNF receptor family members, TACI and BCMA. We show that mice treated with TACI-Ig and TACI-Ig transgenic mice have fewer transitional T2 and mature B cells and reduced levels of circulating immunoglobulin. TACI-Ig treatment inhibits both the production of collagen-specific Abs and the progression of disease in a mouse model of rheumatoid arthritis. In BLyS-deficient mice, B cell development is blocked at the transitional T1 stage such that virtually no mature B cells are present, while B-1 cell numbers are relatively normal. These findings further elucidate the roles of BLyS and APRIL in modulating B cell development and suggest that BLyS is required for the development of most but not all mature B cell populations found in the periphery. |
