Cited by 241Psoriasis: Treatment and PathogenesisT-cell and B-cell ImmunologyIL-33, ST2, and ILC Pathways

Th17 cells: from precursors to players in inflammation and infection

Open access
Awasthi, A., Kuchroo, V. K.·2009·International Immunology

Abstract

Upon activation, naive CD4(+) T cells differentiate into different lineages of effector T(h) subsets. Each subset is characterized by its unique cytokine profile and biological functions. T(h)17, a newly described T(h) subset that produces IL-17, IL-17F and IL-22 in preference to other cytokines, has been shown to play an important role in clearing specific pathogens and in inducing autoimmune tissue inflammations. Over the last 2-3 years, significant progress has been made to understand the development and biological functions of T(h)17 subset. Transforming growth factor beta (TGF) together with IL-6 or IL-21 initiates the differentiation while IL-23 stabilizes the generation of T(h)17 cells. The transcription factors of T(h)17 cells [retinoid-related orphan receptor (ROR) gammat, ROR-alpha and signal transducer and activator of transcription-3] have been described recently. Since TGF-beta is essential for the generation of both T(h)17 and regulatory T (T(reg)) cells from naive T cells, which suggests a developmental link between T(h)17 and T(reg) cells. Functions of these two subsets of T cells are, however, opposite to each other; T(h)17 cells are highly pathogenic during the inflammatory process while T(reg) cells are crucial for inhibiting tissue inflammation and maintaining self-tolerance. Here, we review the recent information on differentiation and effector functions of T(h)17 cells during inflammatory conditions.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1093/intimm/dxp021

Cites

13 of 13 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Not all TH17 cells are pathogenic.

    “Not all TH17 cells are pathogenic though (Awasthi and Kuchroo, 2009)”
  • TH17 cells have been proposed to exist in 3 lineages: CCR6-dependent effector cells, memory cells, or IL-23R- and CXCR5-dependent follicular TH17 cells.

    “TH17 cells have been proposed to exist in 3 lineages: CCR6-dependent effector cells, memory cells, or IL-23R- and CXCR5-dependent follicular TH17 cells (Awasthi and Kuchroo, 2009; Sundrud and Trivigno, 2013).”

    From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Awasthi and Kuchroo, 2009

    The Introduction and Concluding remarks describe Th17 as an effector T-helper subset, while 'Interplay between induced Treg and Th17 cells' discusses IL-23R expression in activated effector or memory T cells. Our copy does not propose three Th17 lineages or identify CCR6-dependent effector cells and IL-23R/CXCR5-dependent follicular Th17 cells as those lineages (searched: the three-lineage description, CCR6, CXCR5, and follicular Th17). (LLM, conf=0.75)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 5

  1. 34 Kulkarni, A. B., Huh, C. G., Becker, D. et al. 1993. Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death. Proc. Natl Acad. Sci. USA 90:770.
  2. 43 Korn, T., Mitsdoerffer, M., Croxford, A. L. et al. 2008. IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3 + regulatory T cells. Proc. Natl Acad. Sci. USA 105:18460.
  3. 51 Huber, M., Brustle, A., Reinhard, K. et al. 2008. IRF4 is essential for IL-21-mediated induction, amplification, and stabilization of the Th17 phenotype. Proc. Natl Acad. Sci. USA 105:20846.
  4. 63 Spolski, R., Kashyap, M., Robinson, C., Yu, Z. and Leonard, W. J. 2008. IL-21 signaling is critical for the development of type I diabetes in the NOD mouse. Proc. Natl Acad. Sci. USA 105:14028.
  5. 80 Chen, Z., Laurence, A., Kanno, Y. et al. 2006. Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells. Proc. Natl Acad. Sci. USA 103:8137.

Cited by

Sorted by citations

Authors
Awasthi, A., & Kuchroo, V. K.
Affiliations
Brigham and Women's Hospital (US)
Venue
International Immunology
Published
2009-03-04
Volume
21
Issue
5
Pages
489-498
ISSN
  • 0953-8178 (ISSN-L)
  • 1460-2377
OpenAlex
W2118773711
Cited by
241
References
13
Citations by year
2026: 2 · 2025: 7 · 2024: 6 · 2023: 9 · 2022: 3 · 2021: 13 · 2020: 8 · 2019: 9 · 2018: 10 · 2017: 19 · 2016: 9 · 2015: 20 · 2014: 18 · 2013: 19 · 2012: 22
FWCI
2.32
Type
journal article
Language
en
Open access
Locations
  • International Immunology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Allergy and Infectious Diseases (R01AI044880, P01AI039671)
  • National Institute of Neurological Disorders and Stroke (P01 NS38037, R01NS046414, P01NS038037, R37NS030843, R01NS035685, R01NS045937)
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, IL-17, IL-17F, IL-22, T cell differentiation, TGF-beta, interleukin-6, IL-21, IL-23, RORγ, RORα, STAT3, regulatory T cells, autoimmune inflammation, infection immunity, self-tolerance, naive CD4+ T cells
MeSH terms
Animals, Cell Differentiation, T-Lymphocytes, Helper-Inducer, Humans, Infections, Inflammation, Transcription Factors, Autoimmunity, T-Lymphocyte Subsets, Cytokines, Transforming Growth Factor beta, Interleukin-17, T-Lymphocytes, Regulatory

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review