Cited by 17IL-33, ST2, and ILC PathwaysAsthma and respiratory diseasesMast cells and histamine

At the bedside: the emergence of group 2 innate lymphoid cells in human disease

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Peebles, R Stokes·2015·Journal of Leukocyte Biology

Abstract

ILC2s have been primarily identified at environmental-mucosal interfaces and can be activated quickly by environmental antigens and pathogens to produce large quantities of IL-5 and IL-13. As a result of the production of these cytokines, ILC2s have been implicated in the host response to allergens, viruses, and parasites. However, the exact role of ILC2s in any human disease state is presently unknown, as specifically eliminating these cells is not possible, given that potentially targetable cell-surface markers are shared with other immune cells. Likewise, selectively and completely inhibiting ILC2 activation is also not currently possible, as several activating cytokines, IL-25, IL-33, and TSLP, act in redundancy or are not specific for ILC2 stimulation. Therefore, at this point, we can only identify the relative abundance of ILC2s in organs and tissue identified as being involved in specific diseases, and the contribution of ILC2s in human disease can only be inferred from mouse studies. Given these limitations, in this article, we will review the studies that have examined the presence of ILC2s in human disease states and speculate on their possible role in disease pathogenesis. The intent of the review is to identify priority areas for basic research based on clinical research insights.

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  • ILC2 are activated quickly by environmental antigens and pathogens to release large quantities of IL-13, suggesting a potential role in pulmonary fibrosis.

    “ILC2 are activated quickly by environmental antigens and pathogens to release large quantities of IL-13, thereby suggesting a potential role in pulmonary fibrosis (123).”

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Authors
Peebles, R. S.
Affiliations
Vanderbilt University (US)
Corresponding author
Peebles, R Stokes
Venue
Journal of Leukocyte Biology
Published
2014-12-16
Volume
97
Issue
3
Pages
469-475
ISSN
  • 0741-5400 (ISSN-L)
  • 1938-3673
OpenAlex
W2319751184
Cited by
17
References
33
Citations by year
2025: 1 · 2024: 1 · 2021: 1 · 2020: 1 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 2 · 2014: 1
FWCI
0.23
Type
journal article
Language
en
Open access
Locations
  • Journal of Leukocyte Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. National Institutes of Health (R01 AI 111820, U19 AI 095227-02, R01 HL 090664-04)
  • Department of Veterans Affairs (2IO1BX000624)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
Keywords
ILC2, IL-5, IL-13, IL-25, IL-33, thymic stromal lymphopoietin, allergic inflammation, parasitic infection, viral infection, mucosal immunity, human disease, pathogenesis
MeSH terms
Animals, Disease, Humans, Immunity, Innate, Lymphocytes, Translational Research, Biomedical

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