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International Immunology Advance Access originally published online on March 4, 2005
International Immunology 2005 17(4):459-467; doi:10.1093/intimm/dxh227
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Published by Oxford University Press on behalf of The Japanese Society for Immunology 2005.

IFN{alpha} enhances human B-cell chemotaxis by modulating ligand-induced chemokine receptor signaling and internalization

Gamal Badr, Gwenoline Borhis, Dominique Treton and Yolande Richard

Institut National de la Santé et de la Recherche Medicale U 131, Institut Paris-Sud sur les Cytokines, 32 rue des Carnets, 92 140, Clamart, France

Correspondence to: Y. Richard; E-mail: yolande.richard{at}ipsc.u-psud.fr

In this study, we show that IFN{alpha} increases the chemotaxis of human B cells to CCL20, CCL21 and CXCL12 in a dose- and time-dependent manner. The effect was maximal with 2000 IU ml–1 IFN{alpha}. It peaked at 24 h and decreased thereafter. At 24 h, IFN{alpha} had increased B-cell chemotaxis to CCL20 by 20 ± 6.2% (n = 9, P < 0.002), to CCL21 by 20 ± 8.5% (n = 14, P < 0.0001) and to CXCL12 by 16.3 ± 4.2% (n = 12, P < 0.003) without changing CCR6, CCR7 or CXCR4 expression. IFN{alpha} enhanced the migration of memory B cells to CCL20, CCL21 and CXCL12 2.6-fold more strongly than that of naive B cells. The triggering of chemokine receptors by their ligands resulted in the activation of phosphatidylinositide-3 kinase (PI3K)/protein kinase B (PKB), inhibitory NF-{kappa}B (I{kappa}B{alpha}) RhoA and extracellular signal-regulated protein kinase 1/2 (ERK1/2). All these effectors except ERK1/2 are crucial for B-cell chemotaxis. IFN{alpha} modulated the requirements for B-cell chemotaxis, which became dependent on ERK1/2, more dependent on PI3K, RhoA and nuclear factor-{kappa}B but less dependent on Gß{gamma} and phospholipase C activation. IFN{alpha} also decreased ligand-induced chemokine receptor internalization in a manner dependent on PI3K/AKT and RhoA but not on I{kappa}B{alpha} and ERK1/2. Our data characterize chemokine receptor signaling in human B cells and clarify the relevance of downstream pathways in B-cell chemotaxis and chemokine receptor internalization. They also suggest that non-class I PI3K are involved in B-cell chemotaxis.

Keywords: CCR6, CCR7, cell migration chemokines, CXCR4

Transmitting editor: T. Kurosaki


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