Increased IL-17 and/or IFN-γ producing T-cell subsets in gut mucosa of long-term-treated HIV-1-infected women
OBJECTIVE:The influence of sex on gut mucosal T-cell response in HIV-1 infection remains largely unknown. We explored whether the frequencies of interferon-γ and/or IL-17 producing naive, T central memory and T effector memory (TEM) CD4 (Th1, Th17) and CD8 T (Tc1, Tc17) cells measured in gut and per...
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Veröffentlicht in: | AIDS (London) 2019-03, Vol.33 (4), p.627-636 |
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Sprache: | eng |
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Zusammenfassung: | OBJECTIVE:The influence of sex on gut mucosal T-cell response in HIV-1 infection remains largely unknown. We explored whether the frequencies of interferon-γ and/or IL-17 producing naive, T central memory and T effector memory (TEM) CD4 (Th1, Th17) and CD8 T (Tc1, Tc17) cells measured in gut and peripheral districts differed between female and male HIV-1-infected patients.
METHODS:Thirty long-term-treated HIV-1-infected individuals were enrolled. The frequencies of Th1, Th17, Tc1, Tc17-cell subsets (single and double) were evaluated by multiparametric flow cytometry in lamina propria lymphocytes and peripheral blood mononuclear cells (PBMC).
RESULTS:A sex-based pattern was recorded in the differences of Th1, Th17, Tc1, Tc17-cell subset (single and double) frequencies between gut and peripheral blood. Female patients had stronger alterations in the gut mucosal T-cell repertoire, especially increased Th1, Th17, and Th1/Th17-cell subset frequencies, compared with the blood district than their male counterparts. Higher naive Tc1, Tc17, Tc1/Tc17, TEM Tc17, and TEM Tc1/Tc17 levels were also recorded in the gut mucosa than in the PBMC of HIV-1-infected women. Males and females also differed in their gut T-cell response, with women being characterized by higher Th1, Th17, Tc1, Tc17, and Th1/Th17 cells subset levels than men. By contrast, only TEM Th1/Th17 and TEM Tc17 in PBMC differed between males and females.
CONCLUSION:Sex-based differences observed in the gut T-cell response of HIV-1-infected patients might contribute to the disease dimorphism. |
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ISSN: | 0269-9370 1473-5571 |
DOI: | 10.1097/QAD.0000000000002122 |