Molecular and Cellular Biology, June 2001, p. 4067-4074, Vol. 21, No. 12
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.12.4067-4074.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Institute of Molecular and Cell Biology, Singapore 117609, Republic of Singapore
Received 18 January 2001/Returned for modification 28 February 2001/Accepted 20 March 2001
B-cell maturation protein (BCMA) is a member of the tumor necrosis
factor (TNF) receptor family and is expressed in B lymphocytes. BCMA
binds two TNF family members, BAFF and APRIL, that stimulate cellular
proliferation. BAFF in particular has been shown to influence B-cell
survival and activation, and transgenic mice overexpressing BAFF have a
lupus-like autoimmune disorder. We have inactivated BCMA in the mouse
germ line. BCMA
/
mice have normal B-cell
development, and the life span of mutant B lymphocytes is
comparable to that of wild-type B cells. The humoral immune
responses of BCMA
/
mice to T-cell-independent antigens
as well as high and low doses of T-cell-dependent antigens are also
intact. In addition, mutant mice have normal splenic architecture, and
germinal centers are formed during an ongoing immune response. These
data suggest a functional redundancy of BCMA in B-cell physiology
that is probably due to the presence of TACI, another TNF
receptor family member that is expressed on B cells and that can also
bind BAFF and APRIL.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|