Sandbox Reserved 1647: Difference between revisions
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Researchers believe that the USP10-dependent T-bet deubiquitination and stabilization can regulate antigen induced immune disorder especially in Th1 specific inflammation. Thus, appropriate decreasing USP10 level may contribute to the T-bet degradation and inflammation attenuation. <ref name="Deubiquitination and stabilization of T-bet by USP10">DOI 10.1016/j.bbrc.2014.05.037</ref> | Researchers believe that the USP10-dependent T-bet deubiquitination and stabilization can regulate antigen induced immune disorder especially in Th1 specific inflammation. Thus, appropriate decreasing USP10 level may contribute to the T-bet degradation and inflammation attenuation. <ref name="Deubiquitination and stabilization of T-bet by USP10">DOI 10.1016/j.bbrc.2014.05.037</ref> | ||
Over the past few years, it has been shown by researchers that the polymorphism of TBX21 could act on nasal polyps and aspirin intolerance too. Patients that cumulate aspirin-intolerance and asthma suffer from bronchoconstriction when using aspririn. This bronchoconstriction is due to the production of cysteinyl leukotrienes, a family of inflammatory mediators, triggered by aspirin intake <ref name=" | Over the past few years, it has been shown by researchers that the polymorphism of TBX21 could act on nasal polyps and aspirin intolerance too. Patients that cumulate aspirin-intolerance and asthma suffer from bronchoconstriction when using aspririn. This bronchoconstriction is due to the production of cysteinyl leukotrienes, a family of inflammatory mediators, triggered by aspirin intake <ref name="Spector SL, Wangaard CH, Farr RS. Aspirin and concomitant idiosyncrasies in adult asthmatic patients. J Allergy Clin Immunol. 1979 Dec;64(6 Pt 1):500-6. doi: 10.1016/0091-6749(79)90059-9. PMID: 512268."></ref>. | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
