Scientists recently identified molecular target that could lead to potential therapies for Asthma.
Researchers at the University of California, San Diego School of Medicine, with collaborators in Korea and Scotland, have identified a novel signaling pathway critical to the immune response of cells associated with the initiation of allergic asthma.
The discovery, they say, could point the way to new therapies that suppress the inflammatory allergic response, offering potential relief to millions of Americans with the chronic lung condition and potentially other allergic diseases.
Specifically, the scientists demonstrated that T helper 2 (Th2) type inflammations in allergic asthma involves dendritic cells (DC), a type of white blood cell, which trigger a reduction in the production of cyclic AMP or cAMP, a key messenger molecule for signaling inside cells.
In mouse models, deletion of the gene that codes for a protein that promotes the production of cAMP resulted in spontaneous bronchial asthma, which shares many similarities with human asthma. Conversely, increasing cAMP levels inhibited the cells' inflammatory response that results in asthma's characteristic symptoms.
The immune response of humans, mice and other vertebrates consists of two fundamental components. The first was the innate immune system, which recognizes and responds to pathogens in an immediate, but generalized, way and does not confer long-lasting immunity.
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The second was the adaptive immune system in which highly specialized T and B cells eliminate or prevent pathogen growth and create immunological memory in case of future encounters with the same pathogen.
The study is published in the the Proceedings of the National Academy of Sciences.
