Blockade of Notch Signalling by y-Secretase Inhibitor in Lung T Cells of Asthmatic XXXX Affects T Cell Differentiation and Pulmonary Inflammation.

@entity32 @entity59 @entity19 @entity565 @entity1711 @entity5234 @entity58 @entity6175 @entity45672
UNASSIGNED: Notch is a single-pass transmembrane receptor protein expressed by T cells, which contributes to the pathogenesis of @entity565 through regulation of the development and differentiation of T cells. y-Secretase inhibitor (GSI) acts as an effective blocker of Notch signalling. The present study aimed to investigate the role of GSI @entity45672 in T cell differentiation and antigen-induced @entity32 . An OVA-induced @entity32 @entity19 model was established. Blockade of Notch signalling was achieved using @entity45672 . The expression of @entity58 , @entity59 , IFN-y, @entity5234 signalling and pro-inflammatory transcription factors in activated lung T cells was evaluated. Finally, the therapeutic effect of @entity45672 was investigated by @entity6175 and @entity1711 staining, real-time PCR and ELISA. The expression of @entity58 and @entity59 decreased and that of IFN-y increased significantly, and the protein expression levels of pro-inflammatory transcription factors reduced in active lung T cells after administration of @entity45672 , compared to the control group. @entity45672 treatment prevented OVA-induced @entity32 and histological changes. The serum and bronchoalveolar lavage fluid (BALF) levels of @entity58 and @entity59 in @entity45672 -treated @entity19 decreased significantly, whereas those of IFN-y increased, relative to the levels in OVA-challenged animals treated with PBS. Our findings indicate that Notch signalling plays an important role in the pathogenesis of @entity565 and that @entity45672 may be a potential therapeutic target for allergen-induced @entity32 .
