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Effector T cell plasticity: flexibility in the face of changing circumstances

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Murphy, Kenneth M, Stockinger, Brigitta·2010·Nature Immunology

Abstract

As more states of CD4 T cell differentiation are uncovered, their flexibility is also beginning to be recognized. Components that control the plasticity of CD4 T cell populations include cellular conditions, clonality, transcriptional circuitry and chromatin modifications. Appearance of cellular flexibility may arise from truly flexible genetic programs or, alternatively, from heterogeneous populations. New tools will be needed to define the rules that allow or prohibit cellular transitions.

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Crossref · 10.1038/ni.1899

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  • Th17 cells show substantially greater plasticity than Th1 and Th2 cells.

    “In contrast to Th1 and Th2 cells, Th17 cells show substantially greater plasticity (19, 23, 65).”

    From T <sub>H</sub> 17 cells require ongoing classic IL-6 receptor signaling to retain transcriptional and functional identity (2020) · cites this paper as [65]

    In “Circuit rules” (page unavailable), the paper suggests that Th17 cells may be less stable than Th1 and Th2 cells, and it describes Th17-to-Th1 conversion. That supports a relative-plasticity comparison, but the paper frames it as a possibility rather than establishing the unqualified claim that Th17 cells show substantially greater plasticity. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • IL-23 has been reported to be a trophic factor for Th17 cells, but IL-23 signaling also promotes the transdifferentiation of Th17 cells to Th1-like cells.

    “IL-23 has been reported to be a trophic factor for Th17 cells (19, 23, 65), but IL-23 signaling also promotes the transdifferentiation of Th17 cells to Th1-like cells (19, 26)”

    From T <sub>H</sub> 17 cells require ongoing classic IL-6 receptor signaling to retain transcriptional and functional identity (2020) · cites this paper as [65]

    The Abstract describes IL-23 as required for IL-17-producing CD4+ T cells, broadly consistent with a supportive role, but does not call it a trophic factor. In “Circuit rules” (page not provided), the paper says TH17 cells can transition to TH1 cells, at least in vitro; it does not say IL-23 signaling promotes that transition. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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Sorted by citations

Authors
Murphy, K. M., & Stockinger, B.
Affiliations
  • Howard Hughes Medical Institute (US)
  • Medical Research Council (GB)
Corresponding author
  • Murphy, Kenneth M
  • Stockinger, Brigitta
Venue
Nature Immunology
Published
2010-07-20
Volume
11
Issue
8
Pages
674-680
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W2070791475
Cited by
482
References
14
Citations by year
2026: 8 · 2025: 8 · 2024: 16 · 2023: 22 · 2022: 22 · 2021: 18 · 2020: 17 · 2019: 28 · 2018: 26 · 2017: 37 · 2016: 36 · 2015: 35 · 2014: 40 · 2013: 44 · 2012: 55
FWCI
4.31
Type
journal article
Language
en
Open access
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Howard Hughes Medical Institute
  • National Institute of Allergy and Infectious Diseases (R01AI076427)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords
CD4+ T cell differentiation, T cell heterogeneity, clonality, transcriptional circuitry, chromatin modification
MeSH terms
Animals, Cell Differentiation, Chromatin, Humans, Transcription Factors, Transcription, Genetic, CD4-Positive T-Lymphocytes, T-Lymphocyte Subsets, Epigenesis, Genetic, Adaptive Immunity

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