Souheil Antoine Younes

TL;DR: The data favor a model whereby competent HIV-specific Tcm continuously arise in small numbers but under persistent antigenemia are rapidly induced to differentiate into IFN-γ only–producing cells that lack self-renewal capacity.

TL;DR: Low frequencies of HIV-specific CD4+ T cells persist in the peripheral blood during viremia, are not replicatively senescent, and proliferate when IL-2 is provided exogenously.

TL;DR: It is shown that the loss of proliferative HIV-specific CD4+ T cell responses is associated with the systemic progression of the disease and that a brief exposure to HIV does not allow the establishment of detectable frequencies of HIV- specific memory T cells.

TL;DR: The findings that memory CD4+ T cells and plasma samples of INRs are enriched in gut-derived bacterial solutes p-cresol sulfate (PCS) and indoxyl sulfates (IS) that both negatively correlated with CD4- T cell counts are reported.

TL;DR: A novel SAG/MHCII/TCR architecture is revealed in which vSAGs coerce a near-canonical docking between MHC II and TCR that allows eschewing of traditional CDR3 binding with the associated peptide in favor of MHCII α-chain binding.