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The inhibition of CD4+ T cell proinflammatory response by lactic acid is independent of monocarboxylate transporter 1
Scandinavian Journal of Immunology ( IF 3.7 ) Pub Date : 2021-09-15 , DOI: 10.1111/sji.13103
Peng Yang 1, 2 , Ying Sun 1, 2 , Min Zhang 2 , Linhan Hu 1 , Xinwei Wang 1 , Longlong Luo 2 , Qiao Chunxia 2 , Wang Jing 2 , He Xiao 2 , Xinying Li 2 , Jiannan Feng 2 , Yuanqiang Zheng 1 , Yu Chen 3 , Yanchun Shi 1 , Guojiang Chen 2
Affiliation  

Lactic acid was originally a by-product of glucose metabolism, but many studies have shown that lactic acid plays a vital role in regulating immune cell polarization, differentiation and effector functions. In this study, we provide evidence that lactic acid and low pH impaired the effector function of CD4+ T cells in response to TCR and non-TCR stimulation. Specifically, lactic acid or hydrochloric acid treatment significantly decreased IL-2 and IFN-γ production as well as CD25/CD69 expression. Furthermore, although MCT1 was required for the suppression of CD25 and CD69 expression by lactic acid, using pharmacological inhibition and genetic deletion, we demonstrated that it was dispensable for lactic acid-mediated inhibition of IL-2 and IFN-γ production.

中文翻译:

乳酸对 CD4+T 细胞促炎反应的抑制与单羧酸转运蛋白 1 无关

乳酸最初是葡萄糖代谢的副产物,但许多研究表明,乳酸在调节免疫细胞极化、分化和效应器功能方面起着至关重要的作用。在这项研究中,我们提供证据表明乳酸和低 pH 值损害了 CD4 + T 细胞响应 TCR 和非 TCR 刺激的效应子功能。具体而言,乳酸或盐酸处理显着降低了 IL-2 和 IFN-γ 的产生以及 CD25/CD69 的表达。此外,虽然 MCT1 是由乳酸抑制 CD25 和 CD69 表达所必需的,但使用药理学抑制和基因缺失,我们证明它对于乳酸介导的 IL-2 和 IFN-γ 产生的抑制是不必要的。
更新日期:2021-11-23
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