Figure 2.

Hallmarks of premature senescent T lymphocytes. Chronic inflammation and persistent antigenic stimulation can induce premature senescence of T cells. Premature senescent T lymphocytes express traditional senescent cell characteristics, such as increased DNA damage response (DDR), increased cell cycle arrest protein levels, such as p53, and senescence-associated-β-galactosidase (SA-βgal) activity. In addition, senescent T lymphocytes express specific cell markers, such as the loss of co-stimulatory receptors CD28 and CD27, as well as the loss of the signalosome molecules Zap70 and Lck, involved in the T-cell receptor (TCR) signaling. Furthermore, premature senescent T lymphocytes have a diminished proliferative capacity, low telomerase activity, and altered apoptosis. However, they maintain potent effector functions, including the expression of innate immunity receptors, such as CD11b and CD57, and the co-inhibitory killer cell lectin-like receptor G1 (KLRG1). Recently, it has been proposed that sestrin proteins could be involved in the development of the T-cell senescence phenotype (Created with BioRender.com).