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Tissue-resident memory T cells (T RM ) persist in peripheral tissues for long periods of time in the absence of antigenic stimulation. Upon re-encounter with cognate antigen, T RM  trigger an immediate immune response at the local tissue microenvironment and provide the first line of host defense. T RM  have been reported to play significant roles in host antimicrobial infection, cancer immunotherapy, and pathogenesis of a number of human autoimmune diseases, such as psoriasis, vitiligo, and atopic dermatitis. T RM  display a distinct gene transcriptome with unique gene expression profiles related to cellular metabolism that is different from naive T cells (T N ), central memory T cells (T CM ), and effector memory T cells (T EM ). Skin CD8 +  T RM  upregulate expression of genes associated with lipid uptake and metabolism and utilize mitochondria fatty acid β-oxidation to support their long-term survival (longevity) and function. In this review, we will summarize the recent progresses in the metabolic programming of T RM  and will also discuss the potential to target the unique metabolic pathways of T RM  to treat T RM -mediated diseases.

Metabolic Reprogramming and Longevity of Tissue-Resident Memory T Cells