Alergic inflammation, the role of biologics targeting IL-5 in modulation of adverse inflammation in patients with asthma bronchiale
Abstract
Allergic inflammation is the key component of pathophysiology of bronchial asthma. It is characterized by acumulation of eosinophils in lung tissue which is induced by the presence of abnormal local proinflammatory microenvironment caused by penetration of allergens through impaired epithelial surfaces.
In addition, the proinflammatory environment is also characterized by the presence of damage patterns. The result is abnormal polarisation of T cells to Th2 subset.
T cells of Th2 subset are modulating B cells to produce antibodies, including IgE class. Th2 T cells are able to stimulate local eosinophilopoiesis and activation of eosinophils via various cytokines, including IL-5.
Innate immunity cells, ILC-2, are also participating in these complex mechanisms. The loss of homeostatic regulations can ultimate into the local production of autoantibodies reacting with content of eosinophil cytoplasmatic granules which could be followed by the activation of complement system substantialy contributing to the tissue damage.
Monoclonal antibodies targeting the key component of allergic inflammation, IL-5, are now an integral part of therapy of patients with bronchial asthma. There are substantial differencies both in molecular structure and the way of administration when compared these biologics.
These differencies should be considered when biological therapy is suggested.