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Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
[Research progress on the trans-organ regulation of renal fibrosis by type 3 innate lymphoid cells]
1The First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan 250014, China.
Abstract:
Type 3 innate lymphoid cells (ILC3s) are a subset of innate immune cells regulated by the transcription factor retinoic acid receptor-related orphan receptor γt (RORγt). They are primarily distributed in the intestinal mucosa and lymphoid tissues, where they secrete cytokines such as interleukin 17(IL-17), IL-22, and granulocyte-macrophage colony-stimulating factor (GM-CSF), playing a crucial role in maintaining intestinal mucosal homeostasis, defending against pathogen invasion, and modulating immune responses. Renal fibrosis (RF) is a pathological process triggered by pathogenic factors such as trauma, infection, inflammation, or metabolic abnormalities. It is characterized by damage to renal parenchymal cells, abnormal deposition of extracellular matrix (ECM), and progressive fibrosis of renal tissue, ultimately leading to irreversible loss of kidney function. Recent studies have revealed that ILC3s not only contribute to intestinal homeostasis but are also involved in the progression of RF. Therefore, this review summarizes the research advances in the mechanisms of ILC3-mediated cross-organ regulation in RF, aiming to provide new perspectives for the prevention and treatment of RF.
