Cutting edge: BAFF regulates CD21/35 and CD23 expression independent of its B cell survival function

被引:132
作者
Gorelik, L
Cutler, AH
Thill, G
Miklasz, SD
Shea, DE
Ambrose, C
Bixler, SA
Su, LH
Scott, ML
Kalled, SL [1 ]
机构
[1] Biogen Idec Inc, Cambridge Ctr 12, Dept Immunol & Inflammat, Cambridge, MA 02142 USA
[2] Biogen Idec Inc, Cambridge Ctr, Dept Gene Express, Cambridge, MA 02142 USA
[3] Biogen Idec Inc, Cambridge Ctr, Dept Gene Discovery, Cambridge, MA 02142 USA
[4] Biogen Idec Inc, Cambridge Ctr, Dept Prot Chem, Cambridge, MA 02142 USA
关键词
D O I
10.4049/jimmunol.172.2.762
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 wildtype 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. The Journal of Immunology, 2004,172:762-766.
引用
收藏
页码:762 / 766
页数:5
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