A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection

摘要

HIV infection affects 37 million people and about 1.7 million are infected annually. Only the RV144 vaccine phase III clinical trial elicited significant protection against HIV-1, but the efficacy of HIV-1 acquisition and immune memory were inadequate. To boost the maintenance of an effective vaccine we studied T stem cell memory (TSCM) and innate immunity. TSCM cells were identified by phenotypic markers of CD4+ CD45RO- CD62L+ CCR7+ CD95+ T cells. They were further characterised by an increase in the IL-2/IL-15 receptors and APOBEC3G anti-viral restriction factors, and decrease in the CCR5 co-receptors and α4β7 mucosal homing integrins. A parallel decrease in these coreceptors and increase in restriction factors were found in CD4+ T cells. We suggest a novel mechanism of dual memory stem cells, associated with corresponding innate immunity, are likely to be activated by endogenous HSP70, the hallmark of cellular stress. Both, memory stem cells and innate immunity need to be optimised to boost the efficacy and immune memory of protection against HIV-1.