Allergic asthma represents the interaction between inflammatory and immune mediation, epithelial airway and other cells. This analysis brings together crucial perspectives in this field. Key studies over the past year show that asthma-like conditions in mice may be developed through close junction breaches in the epithelial cells. Although it has previously been shown that innate lymph lymph cells (ILC) stimulate allergic airway disease, the development of serious allergic diseases in mice has been inhibited. The first bind to the integrin Mac-1 (CD12c/CD18) have now been shown to be fibrinogen cleavage products. The discovery of anti-asthma drug PM-43I, which inhibits STAT5 and STAT6 allergie associated transcription factors in mice, and confirmatory evidence for the effectiveness of antifungal voriconazole agent in human asthma are therapeutically relevant new discoveries in recent years.
Studies in the past year have provided critical new insights into the process of the production of anti-asthmatic drugs that block the factors for STAT and prevent fungal growth in airports through epithelial cells, ILCs and coagulation factors to lead to asthma-like disease expression.