Oral immune dysfunction is associated with the expansion of FOXP3⁺PD-1⁺Amphiregulin⁺ T cells during HIV infection.

ABSTRACT: Residual systemic inflammation and mucosal immune dysfunction persist in people living with HIV, despite treatment with combined anti-retroviral therapy, but the underlying immune mechanisms are poorly understood. Here we report that the altered immune landscape of the oral mucosa of HIV-positive patients on therapy involves increased TLR and inflammasome signaling, localized CD4⁺ T cell hyperactivation, and, counterintuitively, enrichment of FOXP3⁺ T cells. HIV infection of oral tonsil cultures in vitro causes an increase in FOXP3⁺ T cells expressing PD-1, IFN-γ, Amphiregulin and IL-10. These cells persist even in the presence of anti-retroviral drugs, and further expand when stimulated by TLR2 ligands and IL-1β. Mechanistically, IL-1β upregulates PD-1 exp

SUBMITTER: Bhaskaran N 

PROVIDER: S-EPMC8390677 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature