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| 001 | 180112 | ||
| 005 | 20240229145605.0 | ||
| 024 | 7 | _ | |a 10.1126/sciimmunol.abh1873 |2 doi |
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| 100 | 1 | _ | |a Weisshaar, Nina |0 P:(DE-He78)4e185694e1e726dc738bad0a0c41cdd0 |b 0 |e First author |u dkfz |
| 245 | _ | _ | |a Rgs16 promotes antitumor CD8+ T cell exhaustion. |
| 260 | _ | _ | |a Washington, DC |c 2022 |b AAAS |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1698997691_23208 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a #EA:D192#LA:D192# / HI-TRON |
| 520 | _ | _ | |a T cells become functionally exhausted in tumors, limiting T cell-based immunotherapies. Although several transcription factors regulating the exhausted T (Tex) cell differentiation are known, comparatively little is known about the regulators of Tex cell survival. Here, we reported that the regulator of G protein signaling 16 (Rgs-16) suppressed Tex cell survival in tumors. By performing lineage tracing using reporter mice in which mCherry marked Rgs16-expressing cells, we identified that Rgs16+CD8+ tumor-infiltrating lymphocytes (TILs) were terminally differentiated, expressed low levels of T cell factor 1 (Tcf1), and underwent apoptosis as early as 6 days after the onset of Rgs16 expression. Rgs16 deficiency inhibited CD8+ T cell apoptosis and promoted antitumor effector functions of CD8+ T cells. Furthermore, Rgs16 deficiency synergized with programmed cell death protein 1 (PD-1) blockade to enhance antitumor CD8+ T cell responses. Proteomics revealed that Rgs16 interacted with the scaffold protein IQGAP1, suppressed the recruitment of Ras and B-Raf, and inhibited Erk1 activation. Rgs16 deficiency enhanced antitumor CD8+ TIL survival in an Erk1-dependent manner. Loss of function of Erk1 decreased antitumor functions of Rgs16-deficient CD8+ T cells. RGS16 mRNA expression levels in CD8+ TILs of patients with melanoma negatively correlated with genes associated with T cell stemness, such as SELL, TCF7, and IL7R, and predicted low responses to PD-1 blockade. This study uncovers Rgs16 as an inhibitor of Tex cell survival in tumors and has implications for improving T cell-based immunotherapies. |
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| 773 | _ | _ | |a 10.1126/sciimmunol.abh1873 |g Vol. 7, no. 71, p. eabh1873 |0 PERI:(DE-600)2862556-0 |n 71 |p eabh1873 |t Science immunology |v 7 |y 2022 |x 2470-9468 |
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