title: IL-6 receptor (CD126'IL-6R') expression is increased on monocytes and B lymphocytes in HIV infection.
abstract: Interleukin-6 (IL-6) is a multifunctional cytokine, with a wide range of effects on various cell types, including several types of cells involved in immune responses. IL-6 is believed to be involved in the pathogenesis of several diseases and may contribute to AIDS pathogenesis in various ways. Elevated levels of IL-6 occur in HIV infection. The objective of this study was to define the distribution of the expression of the 80-kDa alpha subunit of the IL-6 receptor (CD126'IL-6R') on immune cell subpopulations in HIV-infected subjects. CD126 is responsible for IL-6 binding, and its expression determines which cells respond to this cytokine. An elevated number of monocytes, B cells, and CD4 T cells expressing CD126 were seen in the peripheral circulation of HIV-infected subjects when compared to HIV-seronegative control subjects. Also, an increase in the density of CD126 expression was noted on monocytes. Generally, the observed increases in CD126 did not correlate with CD4 levels in HIV-infected subjects or with disease status, with the exception of CD126 expression on CD8 T cells, which was lower in those HIV-infected subjects that had AIDS. In some cases, increased CD126 expressing cells showed higher levels of STAT3 phosphorylation on exposure to recombinant IL-6. These results indicate that greatly elevated levels of CD126-expressing cells, particularly B cells and monocytes, are seen in HIV infection and suggest that the altered expression of CD126 may contribute directly or indirectly to immune dysfunction and to AIDS pathogenesis in HIV infection.
authors.affiliation: Departments of Microbiology, Immunology & Molecular Genetics, and Obstetrics & Gynecology, UCLA School of Medicine and the Los Angeles Center of the Multicenter AIDS Cohort Study (MACS), Los Angeles, California, 90095, USA.
authors.forename: M
authors.initials: M
authors.lastname: van der Meijden
authors.forename: J
authors.initials: J
authors.lastname: Gage
authors.forename: E C
authors.initials: EC
authors.lastname: Breen
authors.forename: T
authors.initials: T
authors.lastname: Taga
authors.forename: T
authors.initials: T
authors.lastname: Kishimoto
authors.forename: O
authors.initials: O
authors.lastname: Martínez-Maza
mesh_terms: D000328:Adult; D018941:Antigens, CD19; D001402:B-Lymphocytes / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D015658:HIV Infections / Q000097:blood* / Q000378:metabolism; D006801:Humans; D016130:Immunophenotyping; D015850:Interleukin-6 / Q000494:pharmacology; D018950:Lipopolysaccharide Receptors; D008297:Male; D009000:Monocytes / Q000378:metabolism*; D010766:Phosphorylation; D019947:Receptors, Interleukin-6 / Q000096:biosynthesis*; D050796:STAT3 Transcription Factor; D015534:Trans-Activators / Q000378:metabolism
chemical_list: D018941:Antigens, CD19; D004268:DNA-Binding Proteins; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D019947:Receptors, Interleukin-6; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D015534:Trans-Activators