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Cited by 1,074Psoriasis: Treatment and PathogenesisT-cell and B-cell ImmunologyCytokine Signaling Pathways and Interactions

The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo

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McGeachy, Mandy J, Chen, Yi, Tato, Cristina M, Laurence, Arian, Joyce-Shaikh, Barbara, Blumenschein, Wendy M, McClanahan, Terrill K, O'Shea, John J +1 more·2009·Nature Immunology
DOI 10.1038/ni.1698PMC PMC2945605
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Abstract

Interleukin 23 (IL-23) is required for autoimmune inflammation mediated by IL-17-producing helper T cells (T(H)-17 cells) and has been linked to many human immune disorders. Here we restricted deficiency in the IL-23 receptor to defined cell populations in vivo to investigate the requirement for IL-23 signaling in the development and function of T(H)-17 cells in autoimmunity, inflammation and infection. In the absence of IL-23, T(H)-17 development was stalled at the early activation stage. T(H)-17 cells failed to downregulate IL-2 and also failed to maintain IL-17 production or upregulate expression of the IL-7 receptor alpha-chain. These defects were associated with less proliferation; consequently, fewer effector T(H)-17 cells were produced in the lymph nodes and hence available to emigrate to the bloodstream and tissues.

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  • IL-23 is required to maintain and stabilize pathogenic TH17 cells.

    “IL-23 is required to maintain and stabilize pathogenic TH17 cells (McGeachy et al., 2009)”

    From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as McGeachy et al., 2009

    The Discussion says IL-23 is required to generate effector TH17 cells through terminal differentiation, rather than to maintain already-differentiated cells. It also says IL-23 does not appear to be required for the functions of already-generated effector TH17 cells. The Introduction mentions maintenance and stabilization as earlier suggestions, not as the paper’s finding; page numbers were not supplied. (LLM, conf=0.88)

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Authors
McGeachy, M. J., Chen, Y., Tato, C. M., Laurence, A., Joyce-Shaikh, B., Blumenschein, W. M., McClanahan, T. K., O'Shea, J. J., & Cua, D. J.
Affiliations
National Institutes of Health (US)
Corresponding author
Cua, Daniel J
ORCID
Venue
Nature Immunology
Publisher
Springer Science and Business Media LLC
Published
2009-02-01
Volume
10
Issue
3
Pages
314-324
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
DOI
10.1038/ni.1698
PMC
PMC2945605
OpenAlex
W1998895238
Cited by
1,074
References
6
Citations by year
2026: 24 · 2025: 41 · 2024: 51 · 2023: 46 · 2022: 51 · 2021: 53 · 2020: 58 · 2019: 64 · 2018: 59 · 2017: 57 · 2016: 58 · 2015: 69 · 2014: 78 · 2013: 85 · 2012: 70
FWCI
40.27
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institutes of Health (Z99 AR999999)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
IL23R, IL-23, IL-17, interleukin-2, IL-7 receptor alpha chain, autoimmunity, inflammation, infection, T cell proliferation
MeSH terms
Animals, Cell Differentiation, Encephalomyelitis, Autoimmune, Experimental, Female, T-Lymphocytes, Helper-Inducer, Interleukin-2, Lymphocyte Activation, Mice, Inbred C57BL, Toxoplasmosis, Animal, Receptors, Interleukin, Mice, Knockout, Interleukin-17, Cell Proliferation, STAT3 Transcription Factor, Mice

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