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Blood, 15 May 2005, Vol. 105, No. 10, pp. 3965-3971.
Prepublished online as a Blood First Edition Paper on February 1, 2005; DOI 10.1182/blood-2004-08-2992.
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IMMUNOBIOLOGY
Regulation of CXCR3 and CXCR4 expression during terminal differentiation of memory B cells into plasma cells
Gwendolin Muehlinghaus,
Luisa Cigliano,
Stephan Huehn,
Anette Peddinghaus,
Heike Leyendeckers,
Anja E. Hauser,
Falk Hiepe,
Andreas Radbruch,
Sergio Arce, and
Rudolf A. Manz
From the Department for Humoral Immunology, German Rheumatism Research Center, Berlin, Germany; Department of Medicine, Rheumatology and Clinical Immunology, Charité University Hospital, Berlin, Germany; Department of Microbiology and Immunology, University of Buffalo, Buffalo, NY; Department for Research and Development, Miltenyi Biotec, Bergisch Gladbach, Germany; and MRC Centre for Immune Regulation, Division for Immunity and Infection, University of Birmingham, Birmingham, United Kingdom.
C-X-C motif chemokine receptor 3 (CXCR3) and CXCR4 expressed on immunoglobulin G (IgG)–plasma-cell precursors formed in memory immune responses are crucial modulators of the homing of these cells. Here, we studied the regulation of the expression of these chemokine receptors during the differentiation of human memory B cells into plasma cells. We show that CXCR3 is absent on CD27- naive B cells but is expressed on a fraction of memory B cells, preferentially on those coexpressing IgG1. On differentiation into plasma-cell precursors, CXCR3+ memory B cells maintain the expression of this chemokine receptor. CXCR3- memory B cells up-regulate CXCR3 and migrate toward concentration gradients of its ligands only when costimulated with interferon  (IFN-), but not interleukin 4 (IL-4), IL-1 , IL-6, IFN- , IFN-, or tumor necrosis factor (TNF-). In contrast, the differentiation of CXCR4- B cells into plasma cells is generally accompanied by the induction of CXCR4 expression. These results show that lack of CXCR4 expression on plasma-cell precursors is not a limiting factor for plasma-cell homing and that the expression of CXCR3 on memory B cells and plasma-cell precursors is induced by IFN-, provided in human T helper type 1 (Th1)–biased immune responses. Once induced in memory B cells, CXCR3 expression remains part of the individual cellular memory.
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