EXPRESSION OF CELL-ADHESION MOLECULES AT THE SURFACE OF IN-VITRO HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-INFECTED HUMAN MONOCYTES - RELATIONSHIPS WITH TUMOR-NECROSIS-FACTOR-ALPHA, INTERLEUKIN-1-BETA, AND INTERLEUKIN-6 SYNTHESES

Citation
R. Lenaour et al., EXPRESSION OF CELL-ADHESION MOLECULES AT THE SURFACE OF IN-VITRO HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-INFECTED HUMAN MONOCYTES - RELATIONSHIPS WITH TUMOR-NECROSIS-FACTOR-ALPHA, INTERLEUKIN-1-BETA, AND INTERLEUKIN-6 SYNTHESES, AIDS research and human retroviruses, 13(10), 1997, pp. 841-855
Citations number
66
Categorie Soggetti
Immunology,"Infectious Diseases
ISSN journal
08892229
Volume
13
Issue
10
Year of publication
1997
Pages
841 - 855
Database
ISI
SICI code
0889-2229(1997)13:10<841:EOCMAT>2.0.ZU;2-G
Abstract
Further evidence suggests that cell adhesion molecules (CAMs) expresse d on the surface of human immunodeficiency virus type 1 (HIV-l)-infect ed cells are regulated during lentiviral infection, To address this hy pothesis we have investigated the kinetic pattern of CAM expression at the surface of HIV-1(Ba-L)-infected human monocytes during the first 72 hr of infection, A significantly lower expression of CD18 and CD54 as well as a decrease in CD44 expression level were observed at the su rface of infected monocytes when compared with mock-infected cultures, No modification of CD11a, CD11b, CD11c, CD58, and CD62L expression wa s detected, Except for CD18, the expression of which at the cell surfa ce is decreased, no modification of CD44 and CD54 expression was obser ved after heat-inactivated HIV-1 treatment of monocytes, Investigation of soluble forms of CAMs (sCAMs) and cytokine production in the cultu re supernatants of infected monocytes showed a peak of sCD44, TNF-alph a, IL-1 beta, and IL-6 release between 2 and 24 hr after infection, Tr eatment of monocytes with monoclonal antibodies (MAbs) against CAMs sh owed that engagement of some CAMs may trigger TNF-alpha and IL-1 beta production, In addition, pretreatment of infected monocytes with a TNF -alpha synthesis inhibitor, RP 55778, or with MAbs directed against IL -1 beta, confirmed the role of TNF-alpha and IL-1 beta in the regulati on of CD18, CD44, and CD54 expression.