| First Author | Seshasayee D | Year | 2003 |
| Journal | Immunity | Volume | 18 |
| Issue | 2 | Pages | 279-88 |
| PubMed ID | 12594954 | Mgi Jnum | J:82331 |
| Mgi Id | MGI:2652299 | Doi | 10.1016/s1074-7613(03)00025-6 |
| Citation | Seshasayee D, et al. (2003) Loss of TACI causes fatal lymphoproliferation and autoimmunity, establishing TACI as an inhibitory BLyS receptor. Immunity 18(2):279-88 |
| abstractText | BLys , a key cytokine that sustains B cell maturation and tolerance, binds three receptors: BR3, BCMA, and TACI. Results from knockout mice implicate a major functional role for BR3 and a redundant one for BCMA in B cell function. TACI's role is controversial based on defects in TI antibody responses accompanied by B cell hyperplasia in knockout mice. We have presently characterized a precise role for TACI in vivo. TACI(-/-) mice develop fatal autoimmune glomerulonephritis, proteinurea, and elevated levels of circulating autoantibodies. Treatment of B cells with TACI agonistic antibodies inhibits proliferation in vitro and activation of a chimeric receptor containing the TACI intracellular domain induces apoptosis. These results demonstrate the critical requirement for TACI in regulating B cell homeostasis. |
