More than 25 years after the discovery of human immunodeficiency virus (HIV) as the causative agent of AIDS, the mechanisms governing pathogenesis and disease progression are still not fully understood. Indeed, a progressive impairment of the immune system, with alterations that affect both innate and adaptive immunity, characterizes the infection with HIV 1 in humans and with simian immunodeficiency virus (SIV) in macaques. It has been proposed that a state of chronic immune activation contributes to loss of CD4 T cells and to alterations of immune responses, ultimately leading to disease progression. The loss of CD4+CCR5+ T cells in the gut associated lymphoid tissue (GALT) has been well documented both in natural host and in pathogenic models of SIV infection. A decrease in the frequency of Th17 cells, a newly discovered subset of effector T cells involved in the immune response against extracellular bacteria, has been recently described by the applicant, in the mucosa of SIV infected rhesus macaques. Nevertheless the migratory capacity of this T cell subpopulation has not been investigated so far. Chemokines are important mediators of leukocyte trafficking and function, and deregulation of their expression might contribute in part to the pathogenesis of HIV-1/SIV infection. The aim of this project is to investigate the mechanisms that mediate Th17 cells trafficking and activities at mucosal sites together with their decrease in frequency during HIV/SIV infection in order to better understand the pathogenesis of AIDS, in view of generating efficient vaccines.
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