MINI REVIEW article

Front. Immunol.

Sec. T Cell Biology

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1613230

Influences of Metabolism and Lipid Homeostasis on Regulatory vs. Conventional T Cells and Implications for Autoimmunity

Provisionally accepted
  • Institute for Immunology and Department of Molecular Biology & Biochemistry, University of California, Irvine, Irvine, CA, United States

The final, formatted version of the article will be published soon.

Regulatory T cells are essential for suppressing an overactive immune system, especially concerning autoimmune disease, tumor growth, and inflammatory disease. This suppressive nature of regulatory T cells is largely due to their metabolic profiles determined by metabolic reprogramming upon activation and subsequent differentiation. As regulatory T cells tend to process and cycle energy differently from other T cell subsets, we are interested in what metabolic processes support regulatory T cell function. This review will consider how regulatory T cells compare with conventional T cells in terms of their participation in distinct metabolic pathways and how the presence of regulatory T cell-specific molecules influences proliferation and suppressive function. Additionally, this review will identify possible metabolic targets of regulatory T cells that could be targeted for development of autoimmune disease therapies.

Keywords: regulatory T cells, Lipid metabilism, metabolic reprograming, mevalonate (MVA) pathway, mTOR, autoimmune disease

Received: 16 Apr 2025; Accepted: 16 Jun 2025.

Copyright: © 2025 Nguyen, Lee and Walsh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Craig Michael Walsh, Institute for Immunology and Department of Molecular Biology & Biochemistry, University of California, Irvine, Irvine, 92697, CA, United States

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