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Cited by 1,861Psoriasis: Treatment and PathogenesisT-cell and B-cell ImmunologyIL-33, ST2, and ILC Pathways

Phenotypic and functional features of human Th17 cells

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Annunziato, Francesco, Cosmi, Lorenzo, Santarlasci, Veronica, Maggi, Laura, Liotta, Francesco, Mazzinghi, Benedetta, Parente, Eliana, Filì, Lucia +8 more·2007·The Journal of Experimental Medicine
DOI 10.1084/jem.20070663PMC PMC2118657
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Abstract

T helper (Th) 17 cells represent a novel subset of CD4+ T cells that are protective against extracellular microbes, but are responsible for autoimmune disorders in mice. However, their properties in humans are only partially known. We demonstrate the presence of Th17 cells, some of which produce both interleukin (IL)-17 and interferon (IFN)-γ (Th17/Th1), in the gut of patients with Crohn's disease. Both Th17 and Th17/Th1 clones showed selective expression of IL-23R, CCR6, and the transcription factor RORγt, and they exhibited similar functional features, such as the ability to help B cells, low cytotoxicity, and poor susceptibility to regulation by autologous regulatory T cells. Interestingly, these subsets also expressed the Th1-transcription factor T-bet, and stimulation of these cells in the presence of IL-12 down-regulated the expression of RORγt and the production of IL-17, but induced IFN-γ. These effects were partially inhibited in presence of IL-23. Similar receptor expression and functional capabilities were observed in freshly derived IL-17–producing peripheral blood and tonsillar CD4+ T cells. The demonstration of selective markers for human Th17 cells may help us to understand their pathogenic role. Moreover, the identification of a subset of cells sharing features of both Th1 and Th17, which can arise from the modulation of Th17 cells by IL-12, may raise new issues concerning developmental and/or functional relationships between Th17 and Th1.

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  • Th17 and Th22 subsets are pivotal to tackle extracellular pathogens, such as extracellular bacteria and fungi, and they both lack CXCR3 and express CCR6 and CCR4.

    “Th17 and Th22 subsets are pivotal to tackle extracellular pathogens, such as extracellular bacteria and fungi, and they both lack CXCR3 and express CCR6 and CCR4 [152-154].”

    From Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition) (2021) · cites this paper as [152]

    The Results section reports that Th17 clones lack CXCR3-A and CXCR3-B and express CCR6 and elevated CCR4; the Discussion describes a protective role against extracellular bacteria, at least in mice. The paper does not establish those properties or that protective role for Th22 cells, and the cited passages do not specifically address fungi. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • CCR6 expression in human TH17 cells is associated with an increased memory phenotype.

    “CCR6 expression in human TH17 cells is associated with an increased memory phenotype (Acosta-Rodriguez et al., 2007; Annunziato et al., 2007).”

    From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Annunziato et al., 2007

    The Results section reports selective CCR6 expression by human Th17 and Th17/Th1 clones. The Discussion notes that CCR6 occurs on memory, but not naive, T cells and suggests these Th17 subsets may be memory cells that retain CCR6. The paper does not directly show that CCR6 expression is associated with an increased memory phenotype within human Th17 cells. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • IL-23 and RORγt, essential mediators of Th17 differentiation, are required for colitis in multiple studies.

    “However, multiple studies have shown that IL-23 and RORγt, which are essential mediators of Th17 differentiation, are required for colitis [127, 131, 132].”

    From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [127]

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Authors
Annunziato, F., Cosmi, L., Santarlasci, V., Maggi, L., Liotta, F., Mazzinghi, B., Parente, E., Filì, L., Ferri, S., Frosali, F., Giudici, F., Romagnani, P., Parronchi, P., Tonelli, F., Maggi, E., & Romagnani, S.
Affiliations
  • 1Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders (DENOTHE)
  • University of Florence (IT)
ORCID
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2007-07-16
Volume
204
Issue
8
Pages
1849-1861
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.20070663
PMC
PMC2118657
OpenAlex
W2122939321
Cited by
1,861
References
54
Citations by year
2026: 24 · 2025: 34 · 2024: 51 · 2023: 52 · 2022: 65 · 2021: 60 · 2020: 59 · 2019: 89 · 2018: 74 · 2017: 82 · 2016: 111 · 2015: 113 · 2014: 113 · 2013: 111 · 2012: 159
FWCI
60.57
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • Florence Research (University of Florence) (submittedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Keywords
Th17 cells, Crohn's disease, IL-17, interferon-gamma, IL23R, CCR6, T-bet, IL-12, IL-23, regulatory T cells, B cell help, intestinal inflammation, autoimmune disease, T cell differentiation
MeSH terms
Cloning, Molecular, Flow Cytometry, Gene Expression Regulation, Humans, Interferon-gamma, Models, Biological, CD4-Positive T-Lymphocytes, Receptors, Interleukin, Microscopy, Confocal, Interleukin-12, Receptors, Chemokine, Interleukin-17, Cell Proliferation, T-Lymphocytes, Regulatory, Interleukin-23, Receptors, CCR6

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