CHEMOTAXIS AND IL-8 RECEPTOR EXPRESSION IN B-CELLS FROM NORMAL AND HIV-INFECTED SUBJECTS

To date, the activities of the alpha chemokines for human peripheral B cells from normal subjects (N-B cells) or from HIV-infected subjects (HIV-B cells) are not well established, No report on the IL-8R express ion on N-B cells and HIV-B cells has been seen. We report in this work that the alpha chemokines IL-8 and growth-regulatory oncogene-alpha ( GRO-alpha) induce a chemotactic migration of N-B cells and HIV-B cells via stimulating the IL-8RB on these cells. The chemotaxis of N-B cell s can be inhibited by IFN-gamma and IL-2, and augmented by IL-4 and IL -13, whereas TNF-alpha and IL-10 have no influence. The chemotaxis of HIV-B cells can be inhibited by IFN-gamma and IL-2, and augmented by T NF-alpha, IL-4, and IL-10, whereas IL-13 has no influence. IL-8R are e xpressed more abundantly on freshly isolated HIV-B cells than N-B cell s (51% and 15%, respectively). The IL-8R on N-B cells can be downregul ated by IFN-gamma, IL-2, and TNF-alpha (selectively on IL-8RA), and up -regulated by IL-4 and IL-13, whereas IL-10 has no influence. The IL-8 R on HIV-B cells can be down-regulated by IFN-gamma and IL-2, and up-r egulated by TNF-alpha, IL-4, and IL-10, whereas IL-13 has no influence . Importantly, N-B cell and HIV-B cell chemotaxis toward IL-8 and GRO- alpha can be blocked by anti-IL-8RB polyclonal Ab, but not by anti-IL- 8RA polyclonal Ab. Our results demonstrate that IL-8 and GRO-alpha are important inflammatory mediators that stimulate the directional migra tion and recruitment of B lymphocytes. The migratory behavior and the expression of IL-8R on HIV-B cells and some of the reactions to Th1 - and Th2-like cytokines are modified significantly during HIV infection .