Participación de las células Th17 en la patogenia de la infección por el virus de la inmunodeficiencia humana de tipo 1

hiv-1 infection is characterized by a gradual decrease of the immunological competence and a massive depletion of cd4+ t cells, particularly in gut-associated lymphoid tissue, which leads to microbial translocation, contributing to immune hyperactivation, the main pathogenic mechanism during hiv-1 infection. th17 cells are a proinflammatory cd4+ t cell subset, which produce il-17, il-21 and il-22 and play a pivotal role in host defense, mainly in the gastrointestinal tissue, where they promote antimicrobial responses and gut mucosa restoration. although th17 depletion is a hallmark of the progression of the simian and human immunodeficiency viral infections and they have been involved in the pathogenic process in some autoimmune diseases, the role of these cells during hiv-1 infection is not completely understood. considering their functional potential, th17 cells could have a dual role, depending on the stage of hiv infection a patient has reached. currently, most evidence suggests that th17 cells have a beneficial role by promoting gut mucosa recovery, preventing microbial translocation and decreasing immune hyperactivation. however, the pathogenic role of these cells, particularly, increasing viral replication through the production of inflammatory cytokines should not be ruled out. in this review, scientific evidence regarding the role of th17 on the pathogenesis of hiv infection is discussed.