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 Blood, 1 March 2008, Vol. 111, No. 5, pp. 2744-2754.
Prepublished online as a Blood First Edition Paper on January 2, 2008; DOI 10.1182/blood-2007-03-081232.

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Submitted March 22, 2007
Accepted October 30, 2007

BAFF enhances chemotaxis of primary human B cells. A particular synergy between BAFF and CXCL13 on memory B cells

Gamal Badr, Gwenoline Borhis, Eric A Lefevre, Nada Chaoul, Frederique Deshayes, Valerie Dessirier, Genevieve Lapree, Andreas Tsapis, and Yolande Richard*

CEA, Service of Immuno-Virology, DSV/iMETI, University Paris-Sud, Orsay, France
Compton Laboratoty, Institute for Animal health, Compton, United Kingdom
UMR-CNRS 7592, Paris, France
INSERM U841, Centre de Recherche INSERM, Creteil, France

* Corresponding author; email: yolande.richard-clausse{at}cea.fr.

B-cell-activating factor of the TNF family, (BAFF) and a proliferation-inducing ligand (APRIL) regulate B lymphocyte survival and activation. We report that BAFF, but not APRIL, increased the chemotactic response of primary human B cells to CCL21, CXCL12 and CXCL13. The BAFF-induced increase in B cell chemotaxis was totally abolished by blockade of BAFF-R and was strongly dependent on the activation of PI3K/AKT, NF-{kappa}B and p38MAPK pathways. BAFF had similar effects on the chemotaxis of naive and memory B cells in response to CCL21 but increased more strongly that of memory B cells to CXCL13 than that of naive B cells. Our findings indicate a previously unreported role for the BAFF/BAFF-R pair in mature B cell chemotaxis. The synergy between CXCL13 and BAFF produced by stromal cells and follicular dentritic cells may have important implications for B cell homeostasis, the development of normal B cell areas and for the formation of germinal center-like follicles that may be observed in various autoimmune diseases.


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Q. Lai Kwan Lam, O. King Hung Ko, B.-J. Zheng, and L. Lu
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PNAS, September 30, 2008; 105(39): 14993 - 14998.
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