Chemotaxis and IL-8 receptor expression in B cells from normal and HIV- infected subjects

• Published in: The Journal of immunology (1950) Vol. 158; no. 1; pp. 475 - 484
• Main Authors: Jinquan, T, Moller, B, Storgaard, M, Mukaida, N, Bonde, J, Grunnet, N, Black, FT, Larsen, CG, Matsushima, K, Thestrup-Pedersen, K
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 01-01-1997
• Subjects: Adult; AIDS/HIV; B-Lymphocytes - drug effects; B-Lymphocytes - immunology; B-Lymphocytes - metabolism; Chemokine CXCL1; Chemokines - pharmacology; Chemokines, CXC; Chemotactic Factors - pharmacology; Chemotaxis, Leukocyte - drug effects; Chemotaxis, Leukocyte - immunology; Growth Substances - pharmacology; HIV Infections - immunology; human immunodeficiency virus; Humans; Intercellular Signaling Peptides and Proteins; Interleukin-8 - metabolism; Interleukin-8 - pharmacology; Middle Aged; Receptors, Interleukin - biosynthesis; Receptors, Interleukin - immunology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.158.1.475

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 expression 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 cells 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 TNF-alpha, IL-4, and IL-10, whereas IL-13 has no influence. IL-8R are expressed more abundantly on freshly isolated HIV-B cells than N-B cells (51% and 15%, respectively). The IL-8R on N-B cells can be down-regulated 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-8R on HIV-B cells can be down-regulated by IFN-gamma and IL-2, and up-regulated 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 migration 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.