Abstract: It is increasingly recognized that the bronchial asthma is a heterogeneous entity, encompassing a variety of different phenotypes. The identification of specific phenotypes is the key to develop more effective personalised treatment. The earliest attempt to phenotype asthma was proposed classifying into extrinsic and intrinsic subtypes. Clinical asthma is mainly divided into allergic (atopic) and non-allergic (non-atopic) asthma. Other phenotypes are based on trigger factors. Later the phenotyping based on the predominant cellular nature of inflammation: It can be divided into eosinophilic and non-eosinohilic. The non-eosinophilic asthma may be neutrophilic, combined, and paucigranulocytic. The discovery of Ig E represented a major breakthrough in asthma research. Ig E is an immunglobulin that plays a central role in pathomechanisms. Later identify with novel immune phenotypes: T-helper-2 high and T-helper-2 low subtypes. Neutrophilic asthma is mostly dependent of T-helper-17 cell induced mechanisms. The cluster analysis have been used increasingly to identify phenotypes. New data have been identified molecular pathways. However phenotyping of asthma is complex because of the overlap of the various phenotypes. The limitations of the studies need future research. Biomarkers e.g. levels of eosinophils in blood and sputum, exhaled nitric oxide fraction, serum immunglobulin E, serum periostin identify different asthma phenotypes. Orv. Hetil., 2017, 158(13), 491–498.
RAS P21 Protein Activator 3 (RASA3) Specifically Promotes Pathogenic T Helper 17 Cell Generation by Repressing T-Helper-2-Cell-Biased Programs