Liver-Resident NK Cells Control Antiviral Activity of Hepatic T Cells via the PD-1-PD-L1 Axis.
Zhou, Jing; Peng, Hui; Li, Kun; Qu, Kun; Wang, Baohui; Wu, Yuzhang; Ye, Lilin; Dong, Zhongjun; Wei, Haiming; Sun, Rui; Tian, Zhigang.
; 50(2): 403-417.e4, 2019 02 19.
Artigo em Inglês | MEDLINE | ID: mdl-30709740
Bioenergetic Insufficiencies Due to Metabolic Alterations Regulated by the Inhibitory Receptor PD-1 Are an Early Driver of CD8(+) T Cell Exhaustion.
Single-cell RNA-seq reveals TOX as a key regulator of CD8<sup>+</sup> T cell persistence in chronic infection.
Loss of Neurological Disease HSAN-I-Associated Gene SPTLC2 Impairs CD8<sup>+</sup> T Cell Responses to Infection by Inhibiting T Cell Metabolic Fitness.
CD4 T Cell Depletion Substantially Augments the Rescue Potential of PD-L1 Blockade for Deeply Exhausted CD8 T Cells.
The transcription factor c-Myb regulates CD8<sup>+</sup> T cell stemness and antitumor immunity.
A deficiency in nucleoside salvage impairs murine lymphocyte development, homeostasis, and survival.
Production of IL-10 by CD4(+) regulatory T cells during the resolution of infection promotes the maturation of memory CD8(+) T cells.
Subsets of exhausted CD8<sup>+</sup> T cells differentially mediate tumor control and respond to checkpoint blockade.
T cells maintain an exhausted phenotype after antigen withdrawal and population reexpansion.
Tissue-specific differences in PD-1 and PD-L1 expression during chronic viral infection: implications for CD8 T-cell exhaustion.