Fine particulate matter (PM2.5) is a major air pollutant that deposits in the alveolar region and induces oxidative stress, DNA damage, apoptosis, and chronic inflammation. T cell immunosenescence is characterized by increased senescence-associated β-galactosidase activity, p16/p21-associated cell-cycle arrest, impaired proliferation, and acquisition of a senescence-associated secretory phenotype (SASP). However, it remains unclear whether PM2.5-induced T cell dysfunction is mechanistically linked to an immunosenescence program. This study aims to define the relationship between PM2.5-induced T cell dysfunction and immunosenescence using environmentally collected PM2.5 and mouse splenocyte-derived T cells. After dose- and time-dependent PM2.5 exposure, T cell function will be assessed by intracellular cytokine staining of IFN-γ, TNF-α, and IL-2 in CD4+ and CD8+ T cells. In parallel, SA-β-gal activity, p16/p21 expression, CellTrace-based proliferation, and RT-qPCR analysis of senescence- and SASP-related genes will be integrated. A chronic low-dose intranasal exposure model and single-cell RNA sequencing will further be used to validate in vivo immune phenotypes and transcriptional alterations associated with PM2.5 exposure. This study will provide a mechanistic basis for understanding air pollution-associated immunotoxicity.