Abstract

Asthma is a chronic inflammatory disease of the airway characterized by airway hyperresponsiveness, tissue remodeling, and infiltration of immune cells. Although the pathophysiological mechanisms of airway inflammation are not fully understood, significant roles have been described for the complement activation byproducts C3a and C5a anaphylatoxins. It was suggested that generation of C3/C3a contributes to the development of common allergic pathways that enhance airway hyperresponsiveness, eosinophil infiltration, and Th2 cytokine production. [1] Zhang X. Köhl J. A complex role for complement in allergic asthma. Expert Rev Clin Immunol. 2010; 6: 269-277 Crossref PubMed Scopus (63) Google Scholar Conversely, ablation of the C5a and its receptor signaling results in the loss of dendritic cell modulation, which induces dysregulation of Th2-biased immune responses. [1] Zhang X. Köhl J. A complex role for complement in allergic asthma. Expert Rev Clin Immunol. 2010; 6: 269-277 Crossref PubMed Scopus (63) Google Scholar

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