Impact of high‐altitude therapy on type‐2 immune responses in asthma patients

Asthma patients present with distinct immunological profiles, with a predominance of type 2 endotype. The aim of this study was to investigate the impact of high‐altitude treatment on the clinical and immunological response in asthma.

[1]  C. Akdis,et al.  Tight junction, mucin, and inflammasome‐related molecules are differentially expressed in eosinophilic, mixed, and neutrophilic experimental asthma in mice , 2018, Allergy.

[2]  J. Sastre,et al.  Asthma diagnosis using integrated analysis of eosinophil microRNAs , 2018, Allergy.

[3]  A. Sangasapaviliya,et al.  Decreased CRTH2 Expression and Response to Allergen Re-stimulation on Innate Lymphoid Cells in Patients With Allergen-Specific Immunotherapy , 2018, Allergy, asthma & immunology research.

[4]  W. Wen,et al.  ILC2 frequency and activity are inhibited by glucocorticoid treatment via STAT pathway in patients with asthma , 2018, Allergy.

[5]  A. Bergström,et al.  Characterization of asthma in the adolescent population , 2018, Allergy.

[6]  Y. Lee,et al.  Childhood asthma clusters reveal neutrophil‐predominant phenotype with distinct gene expression , 2018, Allergy.

[7]  A. Ramasamy,et al.  Synergistic activation of pro-inflammatory type-2 CD8+ T lymphocytes by lipid mediators in severe eosinophilic asthma , 2018, Mucosal Immunology.

[8]  M. V. van Zelm,et al.  Treatment for moderate to severe atopic dermatitis in alpine and moderate maritime climates differentially affects helper T cells and memory B cells in children , 2018, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[9]  M. Kabesch,et al.  Asthma‐ and IgE‐associated polymorphisms affect expression of TH17 genes , 2018, Allergy.

[10]  P. Busse,et al.  Asthma in the elderly and late‐onset adult asthma , 2018, Allergy.

[11]  P. O'Byrne,et al.  Allergen‐induced Increases in Sputum Levels of Group 2 Innate Lymphoid Cells in Subjects with Asthma , 2017, American journal of respiratory and critical care medicine.

[12]  C. Wennerås,et al.  Differences in eosinophil molecular profiles between children and adults with eosinophilic esophagitis , 2017, Allergy.

[13]  P. Panzner,et al.  Asthma management: A new phenotype‐based approach using presence of eosinophilia and allergy , 2017, Allergy.

[14]  K. Jandl,et al.  The therapeutic potential of CRTH2/DP2 beyond allergy and asthma , 2017, Prostaglandins & other lipid mediators.

[15]  E. Bateman,et al.  Fevipiprant, an oral prostaglandin DP2 receptor (CRTh2) antagonist, in allergic asthma uncontrolled on low-dose inhaled corticosteroids , 2017, European Respiratory Journal.

[16]  O. Akbari,et al.  Regulatory T cells and type 2 innate lymphoid cell‐dependent asthma , 2017, Allergy.

[17]  T. Litman,et al.  The immunoglobulin superfamily member CD200R identifies cells involved in type 2 immune responses , 2017, Allergy.

[18]  C. Janson,et al.  Serum periostin relates to type‐2 inflammation and lung function in asthma: Data from the large population‐based cohort Swedish GA(2)LEN , 2017, Allergy.

[19]  J. Shelhamer,et al.  Dysregulation of lipidomic profile and antiviral immunity in response to hyaluronan in patients with severe asthma. , 2017, The Journal of allergy and clinical immunology.

[20]  O. Kalayci,et al.  Allergy in severe asthma , 2017, Allergy.

[21]  C. Flohr,et al.  Overview of systematic reviews in allergy epidemiology , 2017, Allergy.

[22]  I. Pavord,et al.  Fevipiprant, a prostaglandin D2 receptor 2 antagonist, in patients with persistent eosinophilic asthma: a single-centre, randomised, double-blind, parallel-group, placebo-controlled trial. , 2016, The Lancet. Respiratory medicine.

[23]  I. Agache,et al.  Serum IL‐5 and IL‐13 consistently serve as the best predictors for the blood eosinophilia phenotype in adult asthmatics , 2016, Allergy.

[24]  I. Agache,et al.  Endotypes of allergic diseases and asthma: An important step in building blocks for the future of precision medicine. , 2016, Allergology international : official journal of the Japanese Society of Allergology.

[25]  H. Vliagoftis,et al.  Elevated levels of circulating CD4+CRTh2+ T cells characterize severe asthma , 2016, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[26]  I. Hall,et al.  Efficacy of BI 671800, an oral CRTH2 antagonist, in poorly controlled asthma as sole controller and in the presence of inhaled corticosteroid treatment. , 2015, Pulmonary pharmacology & therapeutics.

[27]  P. Klenerman,et al.  Prostaglandin D2 and leukotriene E4 synergize to stimulate diverse TH2 functions and TH2 cell/neutrophil crosstalk , 2015, The Journal of allergy and clinical immunology.

[28]  C. Brightling,et al.  D prostanoid receptor 2 (chemoattractant receptor–homologous molecule expressed on TH2 cells) protein expression in asthmatic patients and its effects on bronchial epithelial cells , 2015, The Journal of allergy and clinical immunology.

[29]  S. Peters.  Asthma phenotypes: nonallergic (intrinsic) asthma. , 2014, The journal of allergy and clinical immunology. In practice.

[30]  J. Bell,et al.  Heightened response of eosinophilic asthmatic patients to the CRTH2 antagonist OC000459 , 2014, Allergy.

[31]  M. Johansson,et al.  Activation states of blood eosinophils in asthma , 2014, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[32]  R. Geenen,et al.  Problematic severe asthma in children treated at high altitude: tapering the dose while improving control , 2014, The Journal of asthma : official journal of the Association for the Care of Asthma.

[33]  Stacy L. Gelhaus,et al.  Prostaglandin D₂ pathway upregulation: relation to asthma severity, control, and TH2 inflammation. , 2013, The Journal of allergy and clinical immunology.

[34]  W. Paul,et al.  Cutaneous immunosurveillance and regulation of inflammation by group 2 innate lymphoid cells , 2013, Nature Immunology.

[35]  E. Israel,et al.  Lipoxin A4 Regulates Natural Killer Cell and Type 2 Innate Lymphoid Cell Activation in Asthma , 2013, Science Translational Medicine.

[36]  D. Charpin.  High altitude and asthma: beyond house dust mites , 2012, European Respiratory Journal.

[37]  C. Lloyd,et al.  Th17 responses in chronic allergic airway inflammation abrogate regulatory T-cell-mediated tolerance and contribute to airway remodeling , 2012, Mucosal Immunology.

[38]  J. Virchow,et al.  Untangling asthma phenotypes and endotypes , 2012, Allergy.

[39]  E. Bel,et al.  High‐altitude treatment: a therapeutic option for patients with severe, refractory asthma? , 2011, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[40]  S. Narumiya,et al.  Role of prostaglandin D2 receptor DP as a suppressor of tumor hyperpermeability and angiogenesis in vivo , 2008, Proceedings of the National Academy of Sciences.

[41]  G. Miller,et al.  Stress and inflammation in exacerbations of asthma , 2007, Brain, Behavior, and Immunity.

[42]  B. Rueckert,et al.  High‐Altitude Climate Therapy Reduces Local Airway Inflammation and Modulates Lymphocyte Activation , 2006, Scandinavian journal of immunology.

[43]  M. Kosinski,et al.  Asthma Control Test: reliability, validity, and responsiveness in patients not previously followed by asthma specialists. , 2006, The Journal of allergy and clinical immunology.

[44]  Michael G. Hunter,et al.  Prostaglandin D2 Causes Preferential Induction of Proinflammatory Th2 Cytokine Production through an Action on Chemoattractant Receptor-Like Molecule Expressed on Th2 Cells , 2005, The Journal of Immunology.

[45]  A. Szczeklik,et al.  Plasma 9α,11β-PGF2, a PGD2 metabolite, as a sensitive marker of mast cell activation by allergen in bronchial asthma , 2004, Thorax.

[46]  G. Moscato,et al.  Increased CD69 expression on peripheral blood eosinophils after specific inhalation challenge , 2002, Allergy.

[47]  P. Sterk,et al.  Benefits of high altitude allergen avoidance in atopic adolescents with moderate to severe asthma, over and above treatment with high dose inhaled steroids , 2001, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[48]  L. Cosmi,et al.  CRTH2 is the most reliable marker for the detection of circulating human type 2 Th and type 2 T cytotoxic cells in health and disease , 2000 .

[49]  D. McCann,et al.  The role of acute and chronic stress in asthma attacks in children , 2000, The Lancet.

[50]  A. Togias,et al.  Airway hyperresponsiveness in asthma: a problem of limited smooth muscle relaxation with inspiration. , 1995, The Journal of clinical investigation.

[51]  H. Simon,et al.  High altitude climate therapy reduces peripheral blood T lymphocyte activation, eosinophilia, and bronchial obstruction in children with house‐dust mite allergic asthma , 1994, Pediatric pulmonology.

[52]  A. Wardlaw,et al.  CD69 is expressed by human eosinophils activated in vivo in asthma and in vitro by cytokines. , 1993, Immunology.

[53]  P. O'Byrne,et al.  Changes in the cellular profile of induced sputum after allergen-induced asthmatic responses. , 1992, The American review of respiratory disease.

[54]  T. Lee,et al.  Mediator concentrations in bronchoalveolar lavage fluid of patients with mild asymptomatic bronchial asthma. , 1992, The European respiratory journal.

[55]  S. Durham,et al.  Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma. , 1992, The New England journal of medicine.

[56]  C. Akdis,et al.  Type 2 innate lymphoid cells disrupt bronchial epithelial barrier integrity by targeting tight junctions through IL‐13 in asthmatic patients , 2018, The Journal of allergy and clinical immunology.

[57]  M. Idzko,et al.  Regulation of bronchial epithelial barrier integrity by type 2 cytokines and histone deacetylases in asthmatic patients , 2017, The Journal of allergy and clinical immunology.

[58]  D. Broide,et al.  Group 2 innate lymphoid cells: new players in human allergic diseases. , 2015, Journal of investigational allergology & clinical immunology.