Nitric oxide (NO) is a key messenger in the pathogenesis of inflammation, linking innate and adaptive immunity. By targeting signaling molecules, NO from inducible NO synthase (iNOS) and endothelial (e)NOS affects T helper cell differentiation and the effector functions of T lymphocytes, and is a potential target for therapeutic manipulation. In this review we discuss the regulatory actions exerted by NO on T cell functions, focusing on S-nitrosylation as an important post-translational modification by which NO acts as a signaling molecule during T cell-mediated immunity. We also present recent findings showing novel mechanisms through which NO regulates the activation of human T cells, and consider their potential in strategies to treat tumoral, allergic, and autoimmune diseases.

一氧化氮（NO）是炎症发病机理中的关键信使，将先天免疫和适应性免疫联系在一起。通过靶向信号分子，来自诱导型NO合酶（iNOS）和内皮（e）NOS的NO影响T辅助细胞分化和T淋巴细胞的效应子功能，并且是治疗性操作的潜在靶标。在这篇综述中，我们讨论了NO对T细胞功能的调节作用，重点是S-亚硝基化，这是一种重要的翻译后修饰，NO在T细胞介导的免疫过程中作为信号分子起作用。我们还提出了最近的发现，这些发现显示了通过NO调节人类T细胞活化的新机制，并考虑了它们在治疗肿瘤，变态反应和自身免疫性疾病的策略中的潜力。