Metabolic influences on T cell in psoriasis: a literature review.

Front Immunol

Department of Dermatology, Beijing Chao-yang Hospital, Capital Medical University, Beijing, China.

Published: December 2023

AI Article Synopsis

  • Psoriasis is an inflammatory disease that often occurs alongside other health issues like hypertension, diabetes, and inflammatory bowel disease due to similar inflammatory processes and immune system dysfunctions.
  • The review focuses on how metabolites regulate immune cell functions, especially T lymphocytes, and how different metabolic pathways (glucose, lipid, and amino acid) are impacted by psoriasis.
  • It also discusses recent findings in metabolomics to deepen knowledge of psoriasis pathogenesis and to pinpoint potential therapeutic targets through metabolic biomarkers.

Article Abstract

Psoriasis is a systemic inflammatory disease that frequently coexists with various other conditions, such as essential hypertension, diabetes, metabolic syndrome, and inflammatory bowel disease. The association between these diseases may be attributed to shared inflammatory pathways and abnormal immunomodulatory mechanisms. Furthermore, metabolites also play a regulatory role in the function of different immune cells involved in psoriasis pathogenesis, particularly T lymphocytes. In this review, we have summarized the current research progress on T cell metabolism in psoriasis, encompassing the regulation of metabolites in glucose metabolism, lipid metabolism, amino acid metabolism, and other pathways within T cells affected by psoriasis. We will also explore the interaction and mechanism between psoriatic metabolites and immune cells. Moreover, we further discussed the research progress of metabolomics in psoriasis to gain a deeper understanding of its pathogenesis and identify potential new therapeutic targets through identification of metabolic biomarkers associated with this condition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10684739PMC
http://dx.doi.org/10.3389/fimmu.2023.1279846DOI Listing

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