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白细胞介素18在胰腺癌慢性炎症与T细胞耗竭之间的交叉点上

IL18 at the Crossroads between Chronic Inflammation and T-cell Exhaustion in Pancreatic Cancer.

作者信息

Stromnes Ingunn M

机构信息

Center for Immunology, University of Minnesota, Minneapolis, Minnesota.

Department of Microbiology and Immunology, University of Minnesota, Minneapolis, Minnesota.

出版信息

Cancer Immunol Res. 2023 Apr 3;11(4):400. doi: 10.1158/2326-6066.CIR-23-0145.

Abstract

Chronic inflammation and immune evasion are hallmarks of cancer. Cancer promotes T-cell differentiation toward an exhausted, or dysfunctional state, which contributes to immune evasion. In this issue, Lutz and colleagues show that the proinflammatory cytokine IL18 correlates with poor patient prognosis and promotes CD8+ T-cell exhaustion in pancreatic cancer by enhancing IL2R signaling. This link between proinflammatory cytokines and T-cell exhaustion elucidates consequences of modulating cytokine signaling during cancer immunotherapy. See related article by Lutz et al. p. 421 (1) .

摘要

慢性炎症和免疫逃逸是癌症的标志。癌症促使T细胞分化为耗竭或功能失调状态,这有助于免疫逃逸。在本期杂志中,卢茨及其同事表明,促炎细胞因子IL18与患者预后不良相关,并通过增强IL2R信号传导促进胰腺癌中CD8 + T细胞耗竭。促炎细胞因子与T细胞耗竭之间的这种联系阐明了癌症免疫治疗期间调节细胞因子信号传导的后果。见卢茨等人的相关文章,第421页(1)。

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