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Human Asthma Phenotypes: from the Clinic, to Cytokines, and Back Again

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Journal Immunol Rev
Date 2011 Jun 21
PMID 21682748
Citations 66
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Abstract

A large body of experimental evidence supports the hypothesis that T-helper 2 (Th2) cytokines orchestrate allergic airway inflammation in animal models. However, human asthma is heterogeneous with respect to clinical features, cellular sources of inflammation, and response to common therapies. This disease heterogeneity has been investigated using sputum cytology as well as unbiased clustering approaches using cellular and clinical data. Important differences in cytokine-driven inflammation may underlie this heterogeneity, and studies in human subjects with asthma have begun to elucidate these molecular differences. This molecular heterogeneity may be assessed by existing biomarkers (induced sputum evaluation or exhaled nitric oxide testing) or may require novel biomarkers. Effective testing and application of emerging therapies that target Th2 cytokines will depend on accurate and easily obtained biomarkers of this molecular heterogeneity in asthma. Furthermore, whether other non-Th2 cytokine pathways underlie airway inflammation in specific subsets of patients with asthma is an unresolved question and an important goal of future research using both mouse models and human studies.

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References
1.
Cui J, Pazdziorko S, Miyashiro J, Thakker P, Pelker J, DeClercq C . TH1-mediated airway hyperresponsiveness independent of neutrophilic inflammation. J Allergy Clin Immunol. 2005; 115(2):309-15. DOI: 10.1016/j.jaci.2004.10.046. View

2.
Grunig G, Warnock M, Wakil A, Venkayya R, Brombacher F, Rennick D . Requirement for IL-13 independently of IL-4 in experimental asthma. Science. 1998; 282(5397):2261-3. PMC: 3897229. DOI: 10.1126/science.282.5397.2261. View

3.
Crimi E, Spanevello A, Neri M, Ind P, Rossi G, Brusasco V . Dissociation between airway inflammation and airway hyperresponsiveness in allergic asthma. Am J Respir Crit Care Med. 1998; 157(1):4-9. DOI: 10.1164/ajrccm.157.1.9703002. View

4.
Dougherty R, Sidhu S, Raman K, Solon M, Solberg O, Caughey G . Accumulation of intraepithelial mast cells with a unique protease phenotype in T(H)2-high asthma. J Allergy Clin Immunol. 2010; 125(5):1046-1053.e8. PMC: 2918406. DOI: 10.1016/j.jaci.2010.03.003. View

5.
Moorman J, Anne Rudd R, Johnson C, King M, Minor P, Bailey C . National surveillance for asthma--United States, 1980-2004. MMWR Surveill Summ. 2007; 56(8):1-54. View