- Oral presentation
- Open Access
Immunodynamics of Th17 cells in HIV-1 subtype ‘C’ infection
© Vajpayee et al; licensee BioMed Central Ltd. 2012
Published: 4 May 2012
Th17 cells are IL-17 producing CD4-T cells which play a vital role in inflammatory responses, antimicrobial defense and autoimmunity. However, the involvement of Th17 cells in HIV-1 infection especially in subtype-C is not yet identified. Thus through this study we try to dissect the role of Th17 cells in HIV-1 subtype ‘C’ infection.
31 HIV seropositive antiretroviral therapy naïve and 8 HIV uninfected healthy control subjects were recruited and characterized as being early, late or slow progressor. Peripheral blood mononuclear cells were isolated from each study subject and stimulated with HIV-1 subtype ‘C’ gag peptide pool and assessed for IL-17 cytokine producing CD4-T cells using intracellular cytokine staining. All clinical groups were statistically compared by Kruskal-Wallis test and Spearman’s correlation coefficient was calculated for correlation of different variables.
Here we reported that both frequency and functionality of HIV-1 specific Th17 cells were induced in early and slow progressors but were significantly reduced (p<0.001) at late stage of infection in peripheral blood. Also a significant negative correlation (ρ=0.55; P=0.0004) was observed between HIV-1 plasma viral load and gag specific %IL-17 production via CD4-T cells.
This study showcases a comprehensive picture of Th17 cellular dynamics in HIV-1 subtype-C infection. Further, our data establishes that higher frequencies of HIV specific Th17 cells correlates with better control of viral replication and can be used as immune correlate of protection.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.