The plasticity of human Treg and Th17 cells and its role in autoimmunity
Open accessAbstract
CD4(+) T helper cells are a central element of the adaptive immune system. They protect the organism against a wide range of pathogens and are able to initiate and control many immune reactions in combination with other cells of the adaptive and the innate immune system. Starting from a naive cell, CD4(+) T cells can differentiate into various effector cell populations with specialized function. This subset specific differentiation depends on numerous signals and the strength of stimulation. However, recent data have shown that differentiated CD4(+) T cell subpopulations display a high grade of plasticity and that their initial differentiation is not an endpoint of T cell development. In particular, FoxP3(+) regulatory T cells (Treg) and Th17 effector T cells demonstrate a high grade of plasticity, which allow a functional adaptation to various physiological situations during an immune response. However, the plasticity of Treg and Th17 cells might also be a critical factor for autoimmune disease. Here we discuss the recent developments in CD4(+) T cell plasticity with a focus on Treg and Th17 cells and its role in human autoimmune disease, in particular multiple sclerosis (MS).
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Chronic inflammatory cues can destabilize FOXP3 expression, downregulate CD25, and induce phenotypic conversion of Tregs into Teffs, including Th1 and Th17, amplifying inflammation.
“Moreover, chronic inflammatory cues can destabilize FOXP3 expression, downregulate CD25, and induce the phenotypic conversion of Tregs into Teffs, including Th1 and Th17, further amplifying the inflammatory response (Kleinewietfeld and Hafler 2013).”
From The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion (2026) · cites this paper as Kleinewietfeld and Hafler 2013
Section 3.2 describes Tregs acquiring Th1-like or Th17-like features under inflammatory conditions, sometimes with reduced suppressive activity and pro-inflammatory responses. It also links FoxP3 loss to pro-inflammatory cells, but does not establish that chronic inflammatory cues destabilize FOXP3 or downregulate CD25; section 2.2 describes CD25 as a marker of Tregs, not as a marker shown to decline during conversion. (LLM, conf=0.86)
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- Authors
- Kleinewietfeld, M., & Hafler, D. A.
- Affiliations
- Broad Institute (US)
- Venue
- Seminars in Immunology
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 25
- Issue
- 4
- Pages
- 305-312
- ISSN
- 1044-5323 (ISSN-L)
- PMC
- PMC3905679
- OpenAlex
- W2070685885
- Cited by
- 389
- References
- 152
- Citations by year
- 2026: 14 · 2025: 24 · 2024: 34 · 2023: 38 · 2022: 32 · 2021: 46 · 2020: 32 · 2019: 30 · 2018: 33 · 2017: 35 · 2016: 32 · 2015: 27 · 2014: 12
- FWCI
- 2.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Nancy Taylor Foundation for Chronic Diseases
- Multiple Sclerosis Society
- National Institutes of Health (AI039671)
- National Institute of Allergy and Infectious Diseases (U19AI070352, U19AI046130, P01AI045757, R01AI091568, P01AI039671)
- National Institute of Neurological Disorders and Stroke (R37NS024247)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- T cell plasticity, regulatory T cells, Foxp3, Th17 cells, CD4+ T cell differentiation, autoimmune disease, multiple sclerosis, effector T cell differentiation
- MeSH terms
- Animals, Cell Communication, Humans, Multiple Sclerosis, Autoimmunity, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory, Th17 Cells
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