IL-6 receptor (CD126 ' IL-6R ') expression is increased on monocytes and Blymphocytes in HIV infection

Citation
M. Van Der Meijden et al., IL-6 receptor (CD126 ' IL-6R ') expression is increased on monocytes and Blymphocytes in HIV infection, CELL IMMUN, 190(2), 1998, pp. 156-166
Citations number
49
Categorie Soggetti
Immunology
Journal title
CELLULAR IMMUNOLOGY
ISSN journal
00088749 → ACNP
Volume
190
Issue
2
Year of publication
1998
Pages
156 - 166
Database
ISI
SICI code
0008-8749(199812)190:2<156:IR('I'>2.0.ZU;2-1
Abstract
Interleukin-g (IL-6) is a multifunctional cytokine, with a wide range of ef fects on various cell types, including several types of cells involved in i mmune responses. IL-6 is believed to be involved in the pathogenesis of sev eral diseases and may contribute to AIDS pathogenesis in various ways. Elev ated 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 o f the IL-6 receptor (CD126'IL-6R') on immune cell subpopulations in HIV-inf ected subjects. CD126 is responsible for IL-6 binding, and its expression d etermines which cells respond to this cytokine. An elevated number of monoc ytes, B cells, and CD4 T cells expressing CD126 were seen in the peripheral circulation of HIV-infected subjects when compared to HIV-seronegative con trol subjects. Also, an increase in the density of CD126 expression was not ed on monocytes. Generally, the observed increases in CD126 did not correla te with CD4 levels in HIV-infected subjects or with disease status, with th e exception of CD126 expression on CD8 T cells, which was lower in those HN -infected subjects that had AIDS. In some cases, increased CD126 expressing cells showed higher levels of STAT3 phosphorylation on exposure to recombi nant IL-6. These results indicate that greatly elevated levels of CD126-exp ressing cells, particularly B cells and monocytes, are seen in HIV infectio n and suggest that the altered expression of CD126 may contribute directly or indirectly to immune dysfunction and to AIDS pathogenesis in HIV infecti on. (C) 1998 Academic Press.