TIGIT 是 T 细胞和 NK 细胞上发现的一种共抑制受体，在与其配体结合后传递抑制信号。这种相互作用抑制各种信号通路的激活，导致细胞功能衰竭，最终抑制过度的炎症反应或促进肿瘤的免疫逃避。在不同炎症条件下的 T 细胞中，TIGIT 表达失调已被注意到，并根据 T 细胞亚群表现出不同的影响。 TIGIT 主要抑制促炎性 T 细胞的效应功能，维持调节性 T 细胞的抑制功能，并影响 Tfh 成熟。从机制上讲，IL27 诱导的转录因子 c-Maf 和 Blimp-1 被认为是 T 细胞中 TIGIT 表达的关键调节因子。值得注意的是，T 细胞中的 TIGIT 表达与肺部疾病有关，特别是气道炎症性疾病，如肺癌、阻塞性肺病、间质性肺病、结节病和 COVID-19。本综述强调了 TIGIT 在 T 细胞免疫和气道炎症性疾病中的重要性。© 2024。作者获得 Springer Science Business Media, LLC（Springer Nature 旗下公司）的独家许可。

TIGIT, a co-inhibitory receptor found on T cells and NK cells, transmits inhibitory signals upon binding to its ligand. This interaction suppresses the activation of various signaling pathways, leading to functional exhaustion of cells, ultimately dampening excessive inflammatory responses or facilitating immune evasion in tumors. Dysregulated TIGIT expression has been noted in T cells across different inflammatory conditions, exhibiting varying effects based on T cell subsets. TIGIT predominantly restrains the effector function of pro-inflammatory T cells, upholds the suppressive function of regulatory T cells, and influences Tfh maturation. Mechanistically, the IL27-induced transcription factors c-Maf and Blimp-1 are believed to be key regulators of TIGIT expression in T cells. Notably, TIGIT expression in T cells is implicated in lung diseases, particularly airway inflammatory conditions such as lung cancer, obstructive pulmonary disease, interstitial lung disease, sarcoidosis, and COVID-19. This review emphasizes the significance of TIGIT in the context of T cell immunity and airway inflammatory diseases.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.