Abstract
Brucella spp. display many strategies to evade T cells establishing a chronic infection. We previously demonstrated that B. abortus (Ba) induce the apoptosis of T cells. Also, we showed that Ba RNA, a viability-associated PAMP (vita-PAMP), is involved in macrophages’ immune modulation. However, we were unaware if Ba RNA could directly modulate T cell functionality. Our results demonstrate that Ba RNA did not induce T cell apoptosis. Instead, it transiently increased the expression of CD69, an early T cell activation marker; which progressively decreased over time. Moreover, Ba RNA decreased T cell proliferation at late time points. Regarding the functional state of T cells, Ba RNA did not alter the expression of the T cell exhaustion-associated markers PD-1 and CD127, but it decreased the T cell senescence-associated markers CD28 and CD27 expression, together with an increase in CD57, at late time points. Moreover, Ba RNA induced an accumulation of cells in the S phase, concomitant with a reduction in G0/G1 population. This was accompanied by a decrease in IFN-ℽ and IL-2 secretion. Our results indicate that Ba RNA promotes a phenotypic profile consistent with T cell senescence, which may represent an undescribed immune evasion strategy for Ba infection chronicity.