HIV-1 diseases progression associated with loss of Th17 cells in subtype ‘C’ infection

► A loss of Th17 cell subset can be the cause and/or the effect of high viral load. ► IL-17 producing CD4 T cells may help in distinguishing progressive and nonprogressive HIV infection. ► HIV-1 infection not only leads to functional impairment of Th17 cells but also disturbs amplification setup of...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2012-10, Vol.60 (1), p.55-63
Hauptverfasser: Singh, Alpana, Vajpayee, Madhu, Ali, Sharique A., Mojumdar, Kamalika, Chauhan, Neeraj Kumar, Singh, Ravinder
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Sprache:eng
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Zusammenfassung:► A loss of Th17 cell subset can be the cause and/or the effect of high viral load. ► IL-17 producing CD4 T cells may help in distinguishing progressive and nonprogressive HIV infection. ► HIV-1 infection not only leads to functional impairment of Th17 cells but also disturbs amplification setup of this subset. ► HAART helps in partial restoration of Th17 cells in HIV-1 infection. ► Loss of Th17 cells from peripheral blood may lead to diarrhea or vice versa. Th17 cells play a crucial role in host immune response. We examined the role of Th17 cells in HIV-1 ‘subtype-C’ infection and report that HIV-1 specific Th17 cells are induced in early infection and slow progressors but are significantly reduced at late stage of infection. There was a further decline in Th17 cells in late stage subjects with gastrointestinal infections. Additionally, we observed expanded population of IL-21 (needed for Th17 population expansion) producing CD4 T cells in early and slow progressors compared to subjects with late stage infection. A significant positive correlation existed between virus specific IL-17 and IL-21 producing CD4 T cells suggesting that HIV-1 infection induces a demand for Th17 cells. A significant negative correlation between virus specific Th17 cells and HIV-1 plasma viral load (pVL) was also observed, indicating a gradual loss of Th17 cells with HIV-1 disease progression.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2012.06.288