On July 31, 2022, Wu, Di; Hu, Luni; Han, Mengwei; Deng, Yichen; Zhang, Yime; Ren, Guanqun; Zhao, Xingyu; Li, Zongxian; Li, Peng; Zhang, Yinlian; Chen, Shanwen; Li, Jun; Shi, Yanyan; Xue, Jianxin; Wang, Pengyuan; Zhong, Chao published an article.Application of 32462-30-9 The title of the article was PD-1 signaling facilitates activation of lymphoid tissue inducer cells by restraining fatty acid oxidation. And the article contained the following:
Anti-programmed death-1 (PD-1) immunotherapy that aims to restore T cell activity in cancer patients frequently leads to immune-related adverse events such as colitis. However, the underlying mechanism is still elusive. Here, we find that Pdcd1-deficient mice exhibit disrupted gut microbiota and aggravated dextran sulfate sodium (DSS)-induced colitis. In addition to T cells, PD-1 is also substantially expressed in colonic lymphoid tissue inducer (LTi) cells. During DSS-induced colitis, LTi cell activation is accompanied by increased PD-1 expression, whereas PD-1 deficiency results in reduced interleukin-22 (IL-22) production by LTi cells and exacerbated inflammation. Mechanistically, activated LTi cells reprogram their metabolism toward carbohydrate metabolism and fatty acid synthesis, while fatty acid oxidation (FAO) is unchanged. However, PD-1 deficiency leads to significantly elevated FAO in LTi cells, which in turn attenuates their activation and IL-22 production Consistently, FAO suppression efficiently restores IL-22 production in Pdcd1-/- LTi cells. Thus, our study provides unforeseen mechanistic insight into colitis occurrence during anti-PD-1 immunotherapy through LTi cell metabolic reconfiguration. The experimental process involved the reaction of H-Phg(4-OH)-OH(cas: 32462-30-9).Application of 32462-30-9
The Article related to antiprogrammeddeath1 signalling lymphoid tissue inducer cell fatty acid oxidation, Immunochemistry: Immunogenetics and other aspects.Application of 32462-30-9
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