Increased Expression of CD23 (Fcε Receptor II) by Peripheral Blood Monocytes of AIDS Patients

23号公路 单核细胞 CD16 CD64 免疫学 免疫球蛋白E 受体 医学 抗体 免疫系统 内科学 CD3型 CD8型
作者
Lloyd Miller,Kamran Atabai,Maja Nowakowski,Audrey Chan,Martin H. Bluth,Howard Minkoff,Helen G. Durkin
出处
期刊:AIDS Research and Human Retroviruses [Mary Ann Liebert, Inc.]
卷期号:17 (5): 443-452 被引量:11
标识
DOI:10.1089/088922201750102544
摘要

Monocytes expressing the Fcε receptor II (CD23) play important roles in inflammatory and allergic immune responses. We found that peripheral blood monocytes of AIDS patients express increased levels of CD23, compared with monocytes of healthy HIV-1-seronegative individuals (controls) (p < 0.05). We compared expression of monocyte CD23 with expression of monocyte Fcγ receptors (CD16, CD32, CD64), plasma/serum levels of IgE (also IgM, IgG, IgA), and Th1 (IFN-γ) and Th2 (IL-4, IL-10) cytokines. We found that monocyte CD23 expression directly correlated with monocyte CD16 expression (p < 0.01, R = 0.58), which was also increased in AIDS patients; there was no correlation with CD32 or CD64 or with soluble factors in plasma/serum (i.e., IgE, IL-4, IL-10, and IFN-γ). Interestingly, despite the known ability of IL-10 to downregulate monocyte CD23 expression, plasma IL-10 levels were increased in these AIDS patients compared with controls (p < 0.05). We thus evaluated the effect of AIDS and control plasma or rhIL-10 to regulate CD23 expression by monocytes in cultures (24 hr) of healthy human cells ± treatment with anti-IL-10R blocking antibody. We found that anti-IL-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 during the immunopathogenesis of HIV-1 disease. Further, monocyte CD23 expression does not appear to be suppressed by the IL-10-enriched environment in AIDS.
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