preventative. Although all CD4+ T cells gut are severely depleted by HIV, the loss of intestinal Th17 cells in particular has been linked to symptoms of chronic, pathogenic HIV and SIV infection. Microbial translocation is a major factor that contributes to chronic inflammation and immune activation in the context of HIV. In non-pathogenic cases of SIV, microbial translocation is not observed. Th17 cells prevent severe HIV infection by maintaining the intestinal epithelial barrier during HIV infection in the gut. Because of their high levels of CCR5 expression, the coreceptor for HIV, they are preferentially infected and depleted. Thus, it is through Th17 cell depletion that microbial translocation occurs. Additionally, the loss of Th17 cells in the intestine leads to a loss of balance between inflammatory Th17 cells and Treg cells, their anti-inflammatory counterparts. Because of their immunosuppressive properties, they are thought to decrease the anti-viral response to HIV, contributing to pathogenesis. There is more Treg activity compared to Th17 activity, and the immune response to the virus is less aggressive and effective. Revitalizing Th17 cells has been shown to decrease symptoms of chronic infection, including decreased inflammation, and results in improved responses to highly active anti-retroviral treatment (HAART). This is an important finding—microbial translocation general results in unresponsiveness to HAART. Patients continue to exhibit symptoms and do not show as reduced a viral load as expected. In an SIV-rhesus monkey model, it was found that administering IL-21, a cytokine shown to encourage Th17 differentiation and proliferation, decreases microbial translocation by increasing Th17 cell populations. It is hopeful that more immunotherapies targeting Th17 cells could help patients who do not respond well to HAART. In addition, Th17 cells are cellular reservoirs of virus in patients submitted to antiretroviral therapy (in addition to the major cell sanctuary which are follicular Th cells) and should contribute to the latency of the HIV infection (Gosselin et al. J Immunol 2010). Contribution of Th17 cells in Tuberculosis Recent studies have recognized that Th17 T cells may play a role in Tuberculosis. Polyfunctional T cells with Th17 T cell features are depleted in individuals that progress to active TB after infection. In freshly resected lung tissue, from individuals with active or previous TB, CD4+ T cells have been identified that are enriched for IL-17–producing cells, including antigen specific T cells. A cohort study conducted in Peru demonstrated that individuals who progressed to develop active TB after