學生姓名:
李維哲
學期:
108上
摘 要:
Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disorder with a complex etiology and heterogeneous presentation that affects up to 20% of children worldwide. IL-33 is a pro-inflammatory cytokine that plays a pivotal role in allergic disorders. In first report, it treated mice with αIL-33Ab via subcutaneous injection of each DNCB treatment 1 h later from day 1 to day 33 for 14 times. A control group received tacrolimus. Skin lesion and scratching behavior were compared. It revealed that DNCB-induced AD-like mice treated with αIL-33Ab showed improved AD-like symptoms. Eosinophils and mast cells infiltration and serum IgE levels were also significantly reduced by αIL-33Ab. The second report examined the phenotype of IL33tg mice lacking each of these cells. Unexpectedly, AD-like inflammation still developed in Rag2KO IL33tg mice lacking T and B cells. In contrast, when ILC2s were depleted in IL33tg mice via bone marrow transplantation from ILC2-lacking, RORα-deficient mice, the development of AD-like inflammation was almost suppressed. Basophils were accumulated in the inflamed skin of IL33tg mice, and AD-like inflammation was alleviated by the conditional depletion of basophils using anti-FcεRIα antibodies or a Bas-TRECK transgenic mouse system.In these basophil-depleted IL33tg skins, ILC2s were decreased and cytokines and chemokines such as IL-5, IL-13, and CCL5 were reduced. This study suggests that IL-33-induced AD-like inflammation is dependent on innate immune responses that are mediated by ILC2s in concert with basophils, and IL-33 may play an important role in AD with ILC2 and basophil.
摘要.pdf