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The Journal of Immunology, 2004, 172: 762-766.
Copyright © 2004 by The American Association of Immunologists


CUTTING EDGE

Cutting Edge: BAFF Regulates CD21/35 and CD23 Expression Independent of Its B Cell Survival Function

Leonid Gorelik1,*, Anne H. Cutler1,2,*, Greg Thill{dagger}, Steven D. Miklasz*, Dianna E. Shea*, Christine Ambrose{ddagger}, Sarah A. Bixler{ddagger}, Lihe Su§, Martin L. Scott* and Susan L. Kalled3,*

Departments of * Immunology and Inflammation, {dagger} Gene Expression, {ddagger} Gene Discovery, and § Protein Chemistry, Biogen Idec Inc., Cambridge Center, Cambridge, MA 02142

Herein we demonstrate that B cell-activating factor of the TNF family (BAFF), a B cell survival factor, also regulates CD21/35 and CD23 expression. BAFF blockade in wild-type mice down-modulates CD21/35 and CD23 on B cells while survival remains intact, and BAFF exposure causes elevated CD21/35 and CD23 expression. Similar down-modulation is observed in bcl-2-transgenic mice treated with a BAFF inhibitor. This is the first evidence that BAFF has a function independent of B cell survival. Reports using CD21/35 and CD23 expression to assess splenic B cell subsets in BAFF-null mice concluded a lack of B cells beyond the immature stage. Since CD21/35 and CD23 are inadequate for delineating B cell subpopulations in BAFF-null mice, we used expression of BAFF-R and several B cell markers to identify more mature splenic B cells in these mice. These data broaden our understanding of BAFF function and correct the view that BAFF-null mice lack mature B cells.




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