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Peer-reviewedCC BY 4.0Frontiers in Immunology

Epigenomic insights into CD4+ T-cell–mediated pathogenesis in autoimmune diseases

  • Manaka Goto1,2
  • Hiroyuki Teruya2
  • Tomohisa Okamura1,2
  • Keishi Fujio2
  1. 1Department of Functional Genomics and Immunological Diseases, Graduate School of Medicine, The University of Tokyo
  2. 2Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo
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Abstract

T cells are central mediators of autoimmune disease pathogenesis. After developing in the thymus, T cells undergo diverse differentiation programs and acquire specialized effector functions in inflamed tissues. Despite sharing the same genome, T cells adopt diverse phenotypes and functions, highlighting the importance of epigenetic mechanisms in regulating their differentiation and activity; however, these mechanisms remain incompletely understood. Comprehensive epigenetic analyses are therefore essential to elucidate these processes. To date, a wide range of approaches has been applied to T-cell research, including analyses of DNA methylation, histone modifications, chromatin accessibility, transcription factor binding, and three-dimensional chromatin architecture. More recently, rapid advances in single-cell technologies have enabled simultaneous profiling of gene expression and chromatin accessibility in the same cell. In parallel, CRISPR-based approaches have enabled genome-wide functional interrogation in primary human T cells, including analyses of non-coding regulatory regions. Furthermore, epigenomic approaches are now being applied to spatial analyses and are expected to provide deeper insight into the organization of T-cell states in inflamed tissues. In this mini review, we highlight recent studies that have leveraged these cutting-edge technologies and discuss how they are advancing our understanding of the T-cell–mediated pathogenesis of autoimmune diseases.

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Cite

BibTeXRIS
BibTeX
@article{goto2026epigenomic,
  title = {{Epigenomic insights into CD4+ T-cell–mediated pathogenesis in autoimmune diseases}},
  author = {Manaka Goto and Hiroyuki Teruya and Tomohisa Okamura and Keishi Fujio},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1974558},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1974558/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Epigenomic insights into CD4+ T-cell–mediated pathogenesis in autoimmune diseases
AU  - Manaka Goto
AU  - Hiroyuki Teruya
AU  - Tomohisa Okamura
AU  - Keishi Fujio
PY  - 2026
DA  - 2026/10/27
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1974558
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1974558/full
AB  - T cells are central mediators of autoimmune disease pathogenesis. After developing in the thymus, T cells undergo diverse differentiation programs and acquire specialized effector functions in inflamed tissues. Despite sharing the same genome, T cells adopt diverse phenotypes and functions, highlighting the importance of epigenetic mechanisms in regulating their differentiation and activity; however, these mechanisms remain incompletely understood. Comprehensive epigenetic analyses are therefore essential to elucidate these processes. To date, a wide range of approaches has been applied to T-cell research, including analyses of DNA methylation, histone modifications, chromatin accessibility, transcription factor binding, and three-dimensional chromatin architecture. More recently, rapid advances in single-cell technologies have enabled simultaneous profiling of gene expression and chromatin accessibility in the same cell. In parallel, CRISPR-based approaches have enabled genome-wide functional interrogation in primary human T cells, including analyses of non-coding regulatory regions. Furthermore, epigenomic approaches are now being applied to spatial analyses and are expected to provide deeper insight into the organization of T-cell states in inflamed tissues. In this mini review, we highlight recent studies that have leveraged these cutting-edge technologies and discuss how they are advancing our understanding of the T-cell–mediated pathogenesis of autoimmune diseases.
SN  - 1664-3224
ER  -