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Cited by 1,654

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Type 2 inflammation in asthma — present in most, absent in many

Open access
Fahy, John V.·2015·Nature Reviews Immunology

Abstract

Asthma is one of the most common chronic immunological diseases in humans, affecting people from childhood to old age. Progress in treating asthma has been relatively slow and treatment guidelines have mostly recommended empirical approaches on the basis of clinical measures of disease severity rather than on the basis of the underlying mechanisms of pathogenesis. An important molecular mechanism of asthma is type 2 inflammation, which occurs in many but not all patients. In this Opinion article, I explore the role of type 2 inflammation in asthma, including lessons learnt from clinical trials of inhibitors of type 2 inflammation. I consider how dichotomizing asthma according to levels of type 2 inflammation — into 'T helper 2 (TH2)-high' and 'TH2-low' subtypes (endotypes) — has shaped our thinking about the pathobiology of asthma and has generated new interest in understanding the mechanisms of disease that are independent of type 2 inflammation.

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Metadata

Authors
Fahy, J. V.
Venue
Nature Reviews Immunology
Published
2014-12-23
Volume
15
Issue
1
Pages
57-65
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2061435251
Cited by
1,654
References
3
FWCI
8.39
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Type 2 inflammation in asthma — present in most, absent in many. https://app.cochat.ai/papers/10.1038/nri3786
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Fahy, J. V. (2015). Type 2 inflammation in asthma — present in most, absent in many. Nature Reviews Immunology. https://doi.org/10.1038/nri3786

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.