Ribosomal protein S26 serves as a checkpoint of T-cell survival and homeostasis in a p53-dependent manner

Ribosomal proteins(RPs),which play critical roles in ribosome assembly and protein translation,have been proven to be associated with important physiological and pathological processes,including the regulation of T-cell development and immune-related diseases.1,2,3 A recent study reported that ribosomal protein S26(Rps26),which is a Diamond–Blackfan anemia-associated RP located in the 40S subunit that controls oocyte growth,4,5 may influence multiple different immune phenotypes.6 Moreover,a SNP in the 5′UTR of the Rps26 gene in CD4^(+)and CD8+T cells was implicated in several autoimmune diseases.7 However,the function of Rps26 in T lymphocytes remains unknown.Here,we found that Rps26 was highly expressed in T lymphocytes.We examined a T-cell-specific Rps26 knockout mouse model and reported for the first time that ablation of Rps26 in T cells not only impairs peripheral T-cell homeostasis but also leads to T-cell developmental arrest in the thymus.Mechanistically,Rps26 critically regulates T-cell survival in a p53-dependent manner.These findings reveal the indispensable role of the Rps26-p53 axis in T-cell development and homeostasis.

Intrinsic PD-L1 promotes antitumor activity of CD8^(+)cytotoxic T lymphocytes via in cis interaction with CD80

Dear Editor,Programmed cell death-ligand 1(PD-L1)on tumor cells can inhibit CD8+cytotoxic T lymphocyte(CTL)-mediated antitumor response by trans-engagement with programmed death protein 1(PD-1).Besides tumor cells,PD-L1 is expressed on T cells.However,the intrinsic role of PD-L1 in T cells has not been widely studied.PD-L1 expression is essential for the survival of activated CD8+T cells,and PD-L1 blockade at the contraction stage reduced the number of effector T cells[1].CD8+T cell responses to influenza virus infection were also impaired in PD-L1-deficient mice[2].