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
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
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.