Open AccessExpression patterns of Fcγ receptors, HLA‐DR and selected adhesion molecules on monocytes from normal and HIV‐infected individuals
Author(s) -
LOCHER CH.,
VANHAM G.,
KESTENS L.,
KRUGER M.,
CEUPPENS J. L.,
VINGERHOETS J.,
GIGASE P.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06616.x
Subject(s) - cd11a , cd14 , integrin alpha m , cell adhesion molecule , monocyte , immunology , receptor , biology , cd64 , cd16 , major histocompatibility complex , mhc class ii , microbiology and biotechnology , cd18 , antigen , immune system , cd3 , cd8 , genetics
SUMMARY The expression and co‐expression profiles of functionally important monocyte surface markers were compared between control and HIV + individuals using combined physical gating and dim CD4 expression to delineate the monocytes. The FcγRII (CD32), the MHC class II antigen HLADR and the adhesion molecules CDIIa (LFA‐1α), CD18 and CD54 (ICAM‐1) showed an unimodal distribution. Of these markers, CDI Ia and HLA‐DR were up‐regulated in the HIV + subjects compared with controls. The expression levels of the adhesion molecules correlated with each other in both patients and controls. The CD11b (CR3‐α), CD14, FcγRI, and FcγRIII markers were bimodally distributed. Compared with controls, monocytes from seropositives contained fewer CD bright+ cells, an equal proportion of FcγI bright+ cells, but twice as many FCγ RIII + cells. The expression level of FcγRI and CD11b within their brightly positive subset increased as CD4T cells decreased. Both in patients and controls, co‐expression of bright CD11b, CD14 and FCγRI was shown, whereas the FcγRIII + cells were negative or dim positive for the former triad. We conclude that the expression of two FcγR (I and III), of the adhesion molecules CD11a and CD11b and of HLA‐DR showed particular alterations on monocytes from HIV + subjects. The relationship of these phenotypic observations with altered cytokine profiles and altered monocyte function is discussed.