Stephanie Mousset


Immunotherapy in allergic asthma during viral infections

Principal investigator
Susetta Finotto

Andreas Goldwich

Immunotherapy in allergic asthma during viral infections

Asthma is a chronic inflammatory disorder of the lung that affects about 300 million people worldwide. Major components of this disease are airway hyper-responsiveness (AHR) and airway inflammation which are controlled by allergen-specific T helper type 2 (TH2) cells, especially in allergic asthma which is the most common form of asthma.
Although eosinophils and allergen-specific TH2 cells represent the inflammation observed in many patients with allergic asthma, viral respiratory infection precipitates asthma symptoms in almost all patients with asthma. Rhinovirus is the most common cause of virus-associated asthma exacerbations. How viral infection causes acute asthma, and whether virus-induced asthma requires the presence of TH2 cells is not yet understood.
Allergen-specific immunotherapy has been used for a long time as a desensitizing therapy for allergic diseases by modulation of T-and B-cell responses and related antibody isotypes, migration of eosinophils, basophils and mast cells to tissues as well as release of their mediators.
However, immunotherapy in conjunction with viral infection has not been described so far and is part of this doctoral project. By establishing an experimental mouse model the immunomodulatory effects of a viral infection before or after a desensitizing treatment will be examined and evaluated.
At the same time the analyses will be transferred on human level by participation in a European-wide study called “PreDicta” ( in which the immune response of asthmatic preschool children will be examined.


Figure:Inflammatory mechanism of Asthma. TH2 cytokines which raise the pro­duction of allergen-specific immunoglobulin E (IL-4), support the growth of eosinophils (IL-5) and mast cells (IL-9) and directly cause AHR (IL-13)..





May 2012 99th Annual Meeting of the American Association of Immunologists, Boston, USA
Immunotherapy reduces IL-33 and IL-6 expression in the lung of T-bet deficient mice in an experimental model of allergic asthma