Figure 1.

DNA damage in rheumatoid arthritis (RA) T cells. Deficiency of the cell cycle regulator and DNA repair kinase ataxia telangiectasia mutated (ATM) changes the fate of T cells in patients with RA. ATM^lo T cells bypass the G₂/M cell cycle checkpoint and insufficiently repair DNA double-strand breaks. One of the major consequences is excessive death of the T cells, possibly leading to lymphopenia, proliferative pressure to compensate for the loss, and thus premature aging. DNA-PKcs = DNA-dependent protein kinase, catalytic subunit.