美国洛克菲勒大学Sohail F. Tavazoie小组的论文发现了膳食精氨酸驱动密码子依赖性MHC I类翻译，提高结肠肿瘤发生和呼吸道病毒感染的免疫力。相关论文发表在2026年7月30日出版的《细胞》杂志上。
该课题组人员发现细胞外精氨酸限制，在癌症和感染中观察到，抑制特异性精氨酸tRNAs-直接抑制主要组织相容性复合体I （MHC I类）的翻译和抗原呈递。精氨酸对MHC I类的调节依赖于密码子图像，因为同源密码子突变阻止了MHC I类的调节。饮食精氨酸限制削弱了对流感和SARS-CoV-2的抗病毒免疫，并增加了结肠肿瘤的发生。相反，通过膳食补充或髓系特异性精氨酸酶1缺失增加精氨酸可用性可提高MHC I类蛋白水平，抑制结肠肿瘤发生，改善病毒感染结果。这些疾病调节作用在β2-微球蛋白（B2m）缺乏的小鼠中被消除。因此，单一氨基酸的饮食调节严重影响密码子偏向翻译和MHC i类介导的呼吸道病毒感染和癌症免疫，揭示了精氨酸缺乏的意想不到的机制和疾病危害，并突出了基于氨基酸的翻译调节治疗的潜力。
据悉，氨基酸水平在不同的病理条件下波动。这些氨基酸调节是否通过调节宿主基因表达直接形成病理生理仍不清楚。
附：英文原文
Title: Dietary arginine drives codon-dependent MHC class I translation and improves immunity in colon tumorigenesis and respiratory viral infection
Author: Qiushuang Wu, Lara M. Seydlitz, Vladislav Iakimov, Dennis J. Hsu, Parham Habibzadeh, H. Heinrich Hoffmann, Philip B. Paty, Charles M. Rice, Sohail F. Tavazoie
Issue&Volume: 2026-07-30
Abstract: Amino acid levels fluctuate across diverse pathological conditions. Whether such amino acid modulations directly shape pathophysiology by regulating host gene expression remains unknown. We found that extracellular arginine restriction, observed in cancer and infection, represses specific arginine tRNAs—directly suppressing translation of major histocompatibility complex I (MHC class I) and antigen presentation. Arginine regulation of MHC class I was codon-usage dependent, as synonymous codon mutations prevented MHC class I modulation. Dietary arginine restriction impaired anti-viral immunity against influenza and SARS-CoV-2 and increased colon tumorigenesis. Conversely, increasing arginine availability via dietary supplementation or myeloid-specific arginase 1 deletion enhanced MHC class I protein levels, suppressed colon tumorigenesis, and improved viral infection outcomes. These disease-modulating effects were abolished in β2-microglobulin (B2m)-deficient mice. Thus, dietary modulation of a single amino acid critically influences codon-biased translation and MHC class I-mediated immunity to respiratory viral infections and cancer, revealing an unexpected mechanism and disease hazard for arginine deficiency and highlighting potential for amino acid-based translation modulation therapy.
DOI: 10.1016/j.cell.2026.07.020
Source: https://www.cell.com/cell/abstract/S0092-8674(26)00818-4