Vinicius Nunes Cordeiro Leal, Edione Cristina dos Reis and Alessandra Pontillo
University of S�£o Paulo, Brazil
Posters & Accepted Abstracts: J Immunome Res
HIV+ patients are characterized by a chronic inflammation, in part mediated by IL-1�² constitutive release. Inflammasome assembly leads to the activation of caspase-1 and consequent cleavage and release of IL-1�² and IL-18. NLRP3-inflammasome is responsible for HIV-1 detection in monocytes and dendritic cells, suggesting that it could be involved in the first steps of HIV-1 infection, and in the establishment of chronic inflammation in infected subjects. Our group demonstrated that the gain-of-function 3â��UTR variant rs10754558 in NLRP3 gene confers protection against HIV-1 infection, in part corroborating this hypothesis. On the other hand, it was recently shown that in T CD4+ lymphocytes NLRP-3 could act as a transcription co-factor for IL4 transcription leading to a Th2 polarization. Taking in account that a Th2 increase has been associated with bad prognosis of HIV+ individuals and with progression to AIDS, we hypothesize that NLRP-3 could contribute to HIV pathogenesis not only due to its role in myeloid cells but also in lymphocytes. As the role of NLRP-3 is poorly elucidated in lymphocytes, aim of this study was to evaluate NLRP-3 differential expression, NLRP-3 inflammasome activation and IL-4 induction in distinct lymphocyte populations from healthy (HIV- ) individuals as well as in HIV+ patients. NLRP-3 activity in lymphocytes was then correlated with the differential distribution of inflammasome SNPs in HIV+ cohort. Our results suggested that NLRP-3 could exert a role in lymphocytes dysregulation in HIV+ patients.
Email: vinicius.nunescl@usp.br
