Essential protein against inflammatory diseases

Researchers at the Mount Sinai Health System in the US have made a scientific breakthrough by uncovering the biological mechanisms by which a family of proteins known as histone deacetylases (HDACs) activate immune cells associated with inflammatory bowel disease (IBD). ) and other inflammatory diseases.

Thanks to this progress,could potentially lead to the development of selective HDAC inhibitors. intended for treatment types of IBD such as ulcerative colitis and Crohn’s disease. Lead author Ming-Ming Zhou comments: “Our understandingHDAC class II specific designation in different cell types has been limited, preventing the development of treatments targeting this promising family of drugs.”

The expert adds: “Thanks to our proof-of-concept research, we unravel the mechanisms of class II HDACs, providing important information to explore its therapeutic potential for safer and more effective treatment of diseases.”

Researchers have focused on class IIa HDACs, including HDAC4 and HDAC7 isolated for its role in regulating development and differentiation Th17 cells. These cells are known to produce interleukin-17. (IL-17), and highly inflammatory cytokine associated with a wide range of diseases, including IBD, multiple sclerosis and rheumatoid arthritis.

Because of the link between excessive Th17 cell activity and human disease, scientists have focused on pharmacological or genetic interventions. targeting HDAC4/7 to treat Th17 cell-mediated inflammation.

Lead author Ka Lung Chung notes: “Role of class IIa HDACs in Th1 cells7, and inflammatory diseases are still largely unexplored.” He further explains: “Mechanistically, we found that class IIa HDACs orchestrate both transcriptional activation and gene repression to direct the differentiation process of Th17 cells. “This important discovery deepens our understanding of the previously controversial role of class IIa HDACs in human biology and disease.”

This study identified a potent class IIa HDAC inhibitor, TMP269, which affects Th17 cell differentiation in a mouse model of ulcerative colitis. Thanks to this discovery, the potential Pharmacological inhibition of class IIA HDACs as a therapeutic approach promising to solve the problem Th17-associated inflammatory and autoimmune diseases.