Persistence in Temporary Lung Niches: A Survival Strategy of Lung-Resident Memory CD8(+) T Cells

Takamura, Shiki

There is strong evidence that CD8 + T RM precursors receive bona fide TCR signaling in the peripheral tissues since the cells exhibit high levels of Nur77 expression (9, 59) . However, the molecular mechanisms by which TCR signalinginduced events elicit T RM formation remain unclear. CD4 + T cells produce IL-2 in response to late antigen recognition, and autocrine IL-2 signaling at the memory check point improves memory CD4 T cell survival in the spleen, MLN, and lung, (90) suggesting it as a potential mechanism. Another observation is that inhibition of the mammalian target of rapamycin (mTOR) during the early phase of infection selectively impairs the formation of CD8 + T RM cells in the small intestine, while simultaneously enhancing memory generation in the spleen (118) , suggesting that mTOR expression in response to local reactivation may play a role in the T RM differentiation by modulating the metabolic status. Clearly, a great deal more study is required to understand how local antigen restimulation optimizes CD8 + T RM formation.