The characteristics of Th1/Th2 cytokine receptors on monocytes in untreated patients of long term nonprogressor or chronic HIV infection.
Monocytes/macrophages play crucial roles in immunity to microorganisms and are one of the important targets for human immunodeficiency virus (HIV) infection. The phenotypes and function of monocytes in HIV-infected patients were poorly determined. We herein detected the expression of Th1/Th2 cytokine receptors on monocyte subsets in the untreated HIV-infected patients of either long term nonprogressor (LTNP) or chronic infection (CHI). CD14(+)CD16(-) monocytes were significantly increased and CD14(+)CD16(+) monocytes were reduced in patients of LTNP or CHI compared with healthy control. IL-6R expression on CD14(+)CD16(-) monocytes were decreased in patients of LTNP or CHI, whereas IL-4R and IL-10R expression on both CD14(+)CD16(-) and CD14(+)CD16(+) monocyte subsets were increased in patients with LTNP or CHI, as determined by flow cytometry and real time PCR assays. The decreased IL-6R expression and enhanced IL-4R and IL-10R expression were also observed on CD4(+) T cells of these patients, indicating that these changes in monocytes are not cell-specific. CD14(+)CD16(-) monocytes of HIV-infected patients produced less TNF-α and IL-1β but identical levels of IL-6, and IL-12 as the control after IFN-γ/LPS stimulation. However, in the presence of IL-4 or IL10, CD14(+)CD16(-) monocytes of HIV-infected patients produced more TNF-α, IL-6, IL-12 or Il-1β after IFN-γ/LPS stimulation than the healthy control, supporting the impaired IL-4R and IL-10R signal pathways in patients with LTNP and CHI. Therefore, our present study offered the basic information for the Th1/Th2 cytokine receptor expression and function on monocyte subsets in untreated HIV-infected individuals.
Transplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
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D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D016022:Case-Control Studies; D002478:Cells, Cultured; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism / Q000502:physiology; D015658:HIV Infections / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D053662:Interleukin-4 Receptor alpha Subunit / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology / Q000378:metabolism* / Q000821:virology; D053701:Receptors, Interleukin-10 / Q000378:metabolism*; D019947:Receptors, Interleukin-6 / Q000378:metabolism*; D017741:Survivors; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism; D055815:Young Adult
D015703:Antigens, CD; D016207:Cytokines; C504000:IL4R protein, human; C508603:IL6R protein, human; D018836:Inflammation Mediators; D053662:Interleukin-4 Receptor alpha Subunit; D008070:Lipopolysaccharides; D053701:Receptors, Interleukin-10; D019947:Receptors, Interleukin-6; D007371:Interferon-gamma