title: HIV-1-stimulated expression of CD11/CD18 integrins and ICAM-1: a possible mechanism for extravascular dissemination of HIV-1-infected cells.
abstract: To identify mechanisms which might facilitate emigration of HIV-1-infected cells from the circulation, we studied the effect of HIV-1 infection on T lymphocyte and monocytoid cell expression of molecules involved in adherence and translocation of leukocytes across endothelial cell barriers. CD11a, CD18, and ICAM-1 were demonstrated on up to 80% of HIV-1-infected H9 T cells by flow cytometry; these molecules were not evident on uninfected H9. CD18 mRNA was detected in HIV-infected, but not in uninfected H9 T cells. Cell surface expression of CD11a and CD18, but not ICAM-1, was increased on HIV-infected, as compared to uninfected U937 and THP1 monocytoid cells. Increased cell surface expression of the leukocyte integrins was associated with a significantly increased tendency of HIV-infected monocytoid cells to adhere to human umbilical vein endothelial cell monolayers or aggregate homotypically. Preincubating the monocytoid cells with anti-CD18 or anti-CD11a or preincubating endothelial cells with anti-ICAM-1 suppressed these cell to cell interactions. These studies suggest that HIV-1 infection stimulates cell surface expression of molecules involved in leukocyte adherence and transendothelial migration in vitro. Similar mechanisms may influence leukocyte trafficking, in vivo, and may play a role in the localization of HIV-1 infected cells in the central nervous system and other tissues.
authors.affiliation: VA Medical Center, Houston, TX.
authors.forename: R D
authors.initials: RD
authors.lastname: Rossen
authors.forename: C W
authors.initials: CW
authors.lastname: Smith
authors.forename: A H
authors.initials: AH
authors.lastname: Laughter
authors.forename: C A
authors.initials: CA
authors.lastname: Noonan
authors.forename: D C
authors.initials: DC
authors.lastname: Anderson
authors.forename: W M
authors.initials: WM
authors.lastname: McShan
authors.forename: M Y
authors.initials: MY
authors.lastname: Hurvitz
authors.forename: F M
authors.initials: FM
authors.lastname: Orson
mesh_terms: D000943:Antigens, Differentiation / Q000378:metabolism; D018845:CD11 Antigens; D018821:CD18 Antigens; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002460:Cell Line; D004730:Endothelium, Vascular / Q000382:microbiology / Q000503:physiopathology; D015658:HIV Infections / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D015497:HIV-1 / Q000302:isolation & purification / Q000502:physiology*; D006801:Humans; D016023:Integrins / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1; D009420:Nervous System / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D016028:Receptors, Leukocyte-Adhesion / Q000378:metabolism
chemical_list: D000943:Antigens, Differentiation; D018845:CD11 Antigens; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D016023:Integrins; D016028:Receptors, Leukocyte-Adhesion; D018799:Intercellular Adhesion Molecule-1