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B Activation and IL-10 Production
* Department of Immunology, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, CO 80206; and
Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, People’s Republic of China
TALL-1 is a member of the TNF family that is critically involved in
B cell survival, maturation, and progression of lupus-like autoimmune
diseases. TALL-1 has three receptors, including BCMA, TACI, and BAFF-R,
which are mostly expressed by B lymphocytes. Gene knockout studies have
indicated that BAFF-R is the major stimulatory receptor for TALL-1
signaling and is required for normal B cell development. The
intracellular signaling mechanisms of BAFF-R are not known. In this
report, we attempted to identify BAFF-R-associated downstream proteins
by yeast two-hybrid screening. This effort identified TNFR-associated
factor (TRAF)3 as a protein specifically interacting with BAFF-R in
yeast two-hybrid assays. Coimmunoprecipitation experiments indicated
that BAFF-R interacts with TRAF3 in B lymphoma cells and this
interaction is stimulated by TALL-1 treatment. Domain mapping
experiments indicated that both a 6-aa membrane proximal region and the
C-terminal 35 aa of BAFF-R are required for its interaction with TRAF3.
Moreover, overexpression of TRAF3 inhibits BAFF-R-mediated NF-
B
activation and IL-10 production. Taken together, our findings suggest
that TRAF3 is a negative regulator of BAFF-R-mediated NF-B
activation and IL-10 production.
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