Ja. Gross et al., TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease: Impaired B cell maturation in mice lacking BLyS, IMMUNITY, 15(2), 2001, pp. 289-302
BLyS and APRIL have similar but distinct biological roles, mediated through
two known TNF receptor family members, TACI and BCMA. We show that mice tr
eated with TACI-Ig and TACI-Ig transgenic mice have fewer transitional T2 a
nd mature B cells and reduced levels of circulating immunoglobulin. TACI-Ig
treatment inhibits both the production of collagen-specific Abs and the pr
ogression of disease in a mouse model of rheumatoid arthritis. In BLyS-defi
cient 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 r
elatively normal. These findings further elucidate the roles of BLyS and AP
RIL 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.