Specific Enzyme For Treatment Of Autoimmune Disease: New Study

Overview

• Post By : Kumar Jeetendra


• Source: Federation of American Societies for Experimental Biology


• Date: 30 Apr,2016

Researcher from Federation of American Societies for Experimental Biology recently study the importance of specific enzyme named salt-inducible kinases for potential importance of treatment of certain autoimmune disease like, Crohn's disease, arthritis, and psoriasis.

The research recently appears in May 2016 issue of Journal of Leukocyte Biology. Researcher suggest that through inhibiting the effect of enzyme salt-inducible kinases Researcher are able to control the release of certain molecules from immune cells responsible for certain autoimmune disorder.

According to Researcher, "Our laboratory studies further expand and validate the potential therapeutic implications of the use of salt-inducible kinase inhibitors for the treatment of immune-mediated inflammatory diseases," said Maria Stella Lombardi, Ph.D., a researcher involved in the work from the University of Geneva in Switzerland. "The development of novel potent, selective, and drug-like inhibitors of the these pathways will allow us in the near future to test them in animal models of chronic inflammatory and autoimmune diseases."

In researcher study scientist used small molecules of two structurally unrelated salt-inducible kinase to confirm that salt-inducible kinase inhibition attenuates proinflammatory cytokine production.

"Inflammatory disorders are one of the largest classes of disease we see in the clinic, but these disorders are very heterogeneous in terms of clinical manifestations and underlying cause," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology.

Note: The above information is for information purposes for more information go through original story source.

Story source: Federation of American Societies for Experimental Biology

Journal References:

M. S. Lombardi, C. Gillieron, D. Dietrich, C. Gabay. SIK inhibition in human myeloid cells modulates TLR and IL-1R signaling and induces an anti-inflammatory phenotype. Journal of Leukocyte Biology, 2015; 99 (5): 711 DOI: 10.1189/jlb.2A0715-307R