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Yang, Riyao; Sun, Linlin; Li, Ching-Fei; Wang, Yu-Han; Yao, Jun; Li, Hui; Yan, Meisi; Chang, Wei-Chao; Hsu, Jung-Mao; Cha, Jong-Ho; Hsu, Jennifer L; Chou, Cheng-Wei; Sun, Xian; Deng, Yalan; Chou, Chao-Kai; Yu, Dihua; Hung, Mien-Chie
Nature communications, 02/2021, Letnik: 12, Številka: 1Journal Article
The two T cell inhibitory receptors PD-1 and TIM-3 are co-expressed during exhausted T cell differentiation, and recent evidence suggests that their crosstalk regulates T cell exhaustion and immunotherapy efficacy; however, the molecular mechanism is unclear. Here we show that PD-1 contributes to the persistence of PD-1 TIM-3 T cells by binding to the TIM-3 ligand galectin-9 (Gal-9) and attenuates Gal-9/TIM-3-induced cell death. Anti-Gal-9 therapy selectively expands intratumoral TIM-3 cytotoxic CD8 T cells and immunosuppressive regulatory T cells (T cells). The combination of anti-Gal-9 and an agonistic antibody to the co-stimulatory receptor GITR (glucocorticoid-induced tumor necrosis factor receptor-related protein) that depletes T cells induces synergistic antitumor activity. Gal-9 expression and secretion are promoted by interferon β and γ, and high Gal-9 expression correlates with poor prognosis in multiple human cancers. Our work uncovers a function for PD-1 in exhausted T cell survival and suggests Gal-9 as a promising target for immunotherapy.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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