CD69 receptor is induced after activation of leukocytes at inflammatory sites. Mice lacking CD69 develop exacerbated forms of inlammatory diseases, which are largely mediated by misbalanced responses of T helper (TH) 17 cells and regulatory T cells (Tregs), indicating that CD69 modulates TH17 differentiation and plays a role in regulatory T cell function. However, the pathophysiological role of CD69 in fibrotic diseases remains largely unknown.
The main goal of this thesis was to gain insights into the involvement of CD69 in peritoneal fibrosis by using CD69 deficient mice in an established peritoneal dialysis mouse model.
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