title: Chemotaxis and IL-8 receptor expression in B cells from normal and HIV-infected subjects.
abstract: 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.
authors.affiliation: Department of Dermatology, University Hospital, Aarhus University, Denmark.
authors.forename: T
authors.initials: T
authors.lastname: Jinquan
authors.forename: B
authors.initials: B
authors.lastname: Møller
authors.forename: M
authors.initials: M
authors.lastname: Storgaard
authors.forename: N
authors.initials: N
authors.lastname: Mukaida
authors.forename: J
authors.initials: J
authors.lastname: Bonde
authors.forename: N
authors.initials: N
authors.lastname: Grunnet
authors.forename: F T
authors.initials: FT
authors.lastname: Black
authors.forename: C G
authors.initials: CG
authors.lastname: Larsen
authors.forename: K
authors.initials: K
authors.lastname: Matsushima
authors.forename: K
authors.initials: K
authors.lastname: Thestrup-Pedersen
mesh_terms: D000328:Adult; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism*; D054360:Chemokine CXCL1; D018925:Chemokines / Q000494:pharmacology; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000494:pharmacology; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000276:immunology*; D006133:Growth Substances / Q000494:pharmacology; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8 / Q000378:metabolism* / Q000494:pharmacology; D008875:Middle Aged; D018123:Receptors, Interleukin / Q000096:biosynthesis* / Q000276:immunology*
chemical_list: C475829:CXCL1 protein, human; D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; D002630:Chemotactic Factors; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8; D018123:Receptors, Interleukin