TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease. impaired B cell maturation in mice lacking BLyS
J A Gross, S R Dillon, S Mudri, J Johnston, A Littau, R Roque, M Rixon, O Schou, K P Foley, H Haugen, S McMillen, K Waggie, R W Schreckhise, K Shoemaker, T Vu, M Moore, A Grossman, C H Clegg, J A Gross, S R Dillon, S Mudri, J Johnston, A Littau, R Roque, M Rixon, O Schou, K P Foley, H Haugen, S McMillen, K Waggie, R W Schreckhise, K Shoemaker, T Vu, M Moore, A Grossman, C H Clegg
Abstract
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.
Source: PubMed