REVIEW
The Th2/Th17 pathway in asthma and the relevant clinical significance
 
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1
Asthma Clinic, Pulmonary Department, Aristotle University of Thessaloniki, George Papanikolaou Hospital, Exochi
 
2
Laboratory of Biological Chemistry, School of Medicine, Faculty of Health Sciences , Aristotle University of Thessaloniki , Thessaloniki, Greece
 
 
Corresponding author
Despoina Papakosta   

Pneumonology Lung Immunology, Pulmonary Department Aristotle University of Thessaloniki, Greece
 
 
Pneumon 2018;31(3):174-182
 
KEYWORDS
ABSTRACT
Asthma is a heterogeneous chronic disease of the airways, characterized by different phenotypes. The principal pathophysiological pathway appears to be Th2 dependent eosinophilic inflammation mainly produced by T helper 2 (Th2) cells. More recently epithelial innate lymphoid cells (ILC2) cell shave been implicated as another source of Th2 cytokines leading to bronchial eosinophilia without previous allergen sensitization. Another pathogenic pathway is the non-Th2 type, mediated by Th1 and especially Th17 lymphocytes, responsible for neutrophilicin flammation. Furthermore, recent studies have associated Th-17 cells with allergic inflammation and eosinophilic asthma. Ongoing clinical trials are expected to further elucidate the role of different cells in the evolution of asthmatic inflammation and also the role of established or novel potential biomarkers in routine clinical practice aiming to maximize drug efficacy in asthmatics. In the present review, we summarize the above mentioned mechanisms focusing on T-helper cell subset plasticity which led to the identification of dual positive Th2/Th17 inflammation.
 
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