Abstract
Recent studies have shown that tight collaboration between pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) is needed to start an innate immune response to allergens. We have investigated whether polymorphisms of innate immunity genes could associate with the susceptibility and clinical phenotypes of bronchial asthma. Thymic stromal lymphopoietin (TSLP) triggers dendritic cell-mediated T helper (Th) 2 inflammatory responses. We have found that promoter polymorphisms including a gain-of-function variant of the TSLP gene are associated with bronchial asthma susceptibility. IL-18 plays multiple roles in chronic inflammation and in a number of infections and enhances both Th-1- and Th-2-mediated immune responses. We have reported that a functionally relevant IL-18 polymorphism contributes to the disease severity of asthma. The variant affects the level of mRNA expression induced by LPS in human monocytes. Further genetic research will contribute to the development of novel diagnostic, therapeutic, and preventive methods for allergic disease.
