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Severe asthma and sinus disease are consequences of type 2 inflammation (T2I), mediated by interleukin (IL)-33 signaling through its membrane-bound receptor, ST2. Inhibiting IL-33 induced lung inflammation may be an effective way to control asthma. Soluble (s)ST2 reduces available IL-33 and limits T2I, but little is known about its regulation.
Recently, A team led by Joshua A. Boyce from Harvard Medical School published an article in the journal Immunity, titled Mast cells control lung type 2 inflammation via prostaglandin E2-driven soluble ST2. It is found that prostaglandin PGE2 can regulate respiratory mucosal mast cells, promote the production of sST2 from mast cells, and inhibit lung inflammation, which provides an important basis for the future treatment of lung inflammation and asthma.
Read more biomedical science news articles at Sungenbiomed.
