Increased expression of CD23 (Fc epsilon receptor II) by peripheral blood monocytes of AIDS patients

Citation
Ls. Miller et al., Increased expression of CD23 (Fc epsilon receptor II) by peripheral blood monocytes of AIDS patients, AIDS RES H, 17(5), 2001, pp. 443-452
Citations number
55
Categorie Soggetti
Immunology
Journal title
AIDS RESEARCH AND HUMAN RETROVIRUSES
ISSN journal
08892229 → ACNP
Volume
17
Issue
5
Year of publication
2001
Pages
443 - 452
Database
ISI
SICI code
0889-2229(20010320)17:5<443:IEOC(E>2.0.ZU;2-V
Abstract
Monocytes expressing the Fc epsilon receptor II (CD23) play important roles in inflammatory and allergic immune responses. We found that peripheral bl ood monocytes of AIDS patients express increased levels of CD23, compared w ith monocytes of healthy HIV-1-seronegative individuals (controls) (p < 0.0 5). We compared expression of monocyte CD23 with expression of monocyte Fc< gamma> receptors (CD16, CD32, CD64), plasma/serum levels of IgE (also IgM, IgG, IgA), and Th1 (IFN-gamma) and Th2 (IL-4, IL-10) cytokines, We found th at monocyte CD23 expression directly correlated with monocyte CD16 expressi on (p < 0.01, R = 0.58), which was also increased in AIDS patients; there w as no correlation with CD32 or CD64 or with soluble factors in plasma/serum (i.e., IgE, IL-4, IL-10, and IFN-<gamma>). Interestingly, despite the know n ability of IL-10 to downregulate monocyte CD23 expression, plasma IL-10 l evels were increased in these AIDS patients compared with controls (p < 0.0 5). We thus evaluated the effect of AIDS and control plasma or rhIL-10 to r egulate CD23 expression by monocytes in cultures (24 hr) of healthy human c ells +/- treatment with anti-IL-10R blocking antibody. We found that anti-I L-10R blocking antibody treatment had no effect on monocyte CD23 expression in cultures containing AIDS plasma, but increased monocyte CD23 expression in cultures containing control plasma (p < 0.05) or rhIL-10. In conclusion , the identification of increased monocyte CD23 expression in AIDS patients may further characterize the aberrant activated phenotype of monocytes dur ing the immunopathogenesis of HIV-1 disease. Further, monocyte CD23 express ion does not appear to be suppressed by the IL-10-enriched environment in A IDS.