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The Journal of Immunology, 1999, 162: 4455-4463.
Copyright © 1999 by The American Association of Immunologists

Antigen Receptor Engagement Selectively Induces Macrophage Inflammatory Protein-1{alpha} (MIP-1{alpha}) and MIP-1ß Chemokine Production in Human B Cells1

Roman Krzysiek, Eric A. Lefèvre, Weiping Zou, Arnaud Foussat, Jérôme Bernard, Alain Portier, Pierre Galanaud and Yolande Richard2

Institut National de la Santé et de la Recherche Médicale, Unit 131, Institut Paris-Sud sur les Cytokines, Clamart, France

We show herein that B cell Ag receptor (BCR) triggering, but not stimulation by CD40 mAb and/or IL-4, rapidly induced the coordinated expression of two closely related T cell chemoattractants, macrophage inflammatory protein-1ß (MIP-1ß) and MIP-1{alpha}, by human B cells. Naive, memory, and germinal center B cells all produced MIP-1{alpha}/ß in response to BCR triggering. In contrast to MIP-1{alpha}/ß, IL-8, which is spontaneously produced by germinal center B cells but not by naive and memory B cells, was not regulated by BCR triggering. Culturing follicular dendritic cell-like HK cells with activated B cells did not regulate MIP-1{alpha} production, but it did induce production of IL-8 by HK cells. Microchemotaxis assays showed that CD4+CD45RO+ T cells of the effector/helper phenotype actively migrated along a chemotactic gradient formed by BCR-stimulated B cells. This effect was partially blocked by anti-MIP-1ß and anti-CC chemokine receptor 5 Ab, but not by anti-MIP-1{alpha} Ab suggesting that MIP-1ß plays a major role in this chemoattraction. Since maturation of the B cell response to a peptide Ag is mostly dependent on the availability of T cell help, the ability of Ag-stimulated B cells to recruit T cells via MIP-1{alpha}/ß, may represent one possible mechanism enabling cognate interactions between rare in vivo Ag-specific T and B cells.




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