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Asthma is a heterogeneous inflammatory airway disease that causes relevant morbidity across individuals of all age cohorts. In recent years, advances in the understanding of asthma pathophysiology have led to the development of treatments tailored to specific pheno- and endotypes of the disease. This has significantly changed asthma management, especially for patients with severe disease. These new treatment options offer individuals with asthma access to personalized and disease-modifying therapies. The present paper is a comprehensive overview of recent clinical studies and of German and international guideline updates on asthma management., Competing Interests: Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht., (Thieme. All rights reserved.)

In the last decades there has been a substantial increase in the prevalence of allergic diseases such as asthma. Hence there is a basic necessity to investigate disease mechanisms of allergic disorders and to trace novel treatment approaches. Indeed, allergic asthma is a disorder which is characterized by airway inflammation, airway obstruction, and hyperresponsiveness. Several of these features can be studied in models of allergic airway disease. In this chapter different mouse models of allergic diseases are described. These include frequently models of allergic airway disease utilizing sensitization and challenge towards ovalbumin. Furthermore a model using the human-relevant allergen-specific house dust mite is described. In addition, information about DC-induced models and analysis of in vitro-generated T cell following transfer into recipients are described as well as analysis of a humanized mouse model is provided.

Similar to T-helper (Th) cells, CD8(+) T cells also differentiate into distinct subpopulations. However, the existence of IL-9-producing CD8(+) T (Tc9) cells has not been elucidated so far. We show that murine CD8(+) T cells activated in the presence of IL-4 plus TGF-β develop into transient IL-9 producers characterized by specific IFN-γ and IL-10 expression patterns as well as by low cytotoxic function along with diminished expression of the CTL-associated transcription factors T-bet and Eomesodermin. Similarly to the CD4(+) counterpart, Tc9 cells required for their differentiation STAT6 and IRF4. Tc9 cells deficient for these master regulators displayed increased levels of Foxp3 that in turn suppressed IL-9 production. In an allergic airway disease model, Tc9 cells promoted the onset of airway inflammation, mediated by subpathogenic numbers of Th2 cells. This support was specific for Tc9 cells because CTLs failed to exert this function. We detected increased Tc9 frequency in the periphery in mice and humans with atopic dermatitis, a Th2-associated skin disease that often precedes asthma. Thus, our data point to the existence of Tc9 cells and to their supportive function in Th2-dependent airway inflammation, suggesting that these cells might be a therapeutic target in allergic disorders., (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)