摘要T cell immune responses are triggered by antigenic peptides presented through major histocompatibility complex class Is(pMHC-Is),which play an important role in the genesis,development,and therapy of tumors.The capacity of a specific pMHC-I to elicit T cell responses is deeply influenced by its expression level(quantity)and its immunogenicity(quality).Tumor cells can evade T cell immunity by down-regulating the quantity of pMHC-Is or selectively eliminating highly immunogenic antigenic peptides.Augmenting the quantity or quality of pMHC-Is is essential for tumor immunotherapy.However,the complexity of pMHC-I regulation and tumor heterogeneity pose challenges to clinical strategies.Consequently,developing approaches grounded in comprehensive analyses of pMHC-I regulatory mechanisms remains a focal point in the research of T cell immunity.In this review,we discuss how tumors modulate their surface pMHC-Is through genetic,epigenetic,and proteomic mechanisms and summarize potential therapeutic strategies targeting these mechanisms,which may provide a valuable reference for the development of novel tumor immunotherapies based on pMHC-I modulation.