<p>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&#039;s disease, arthritis, and psoriasis.</p><p>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.<br /><br /><img src="http://www.microbiozindia.com/images/AZ02.png" alt="" /></p><p>According to Researcher, &amp;quot;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,&amp;quot; said Maria Stella Lombardi, Ph.D., a researcher involved in the work from the University of Geneva in Switzerland. &amp;quot;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.&amp;quot;</p><p>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.</p><p>&amp;quot;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,&amp;quot; said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology.</p><p>Note: The above information is for information purposes for more information go through original story source.</p><p><strong>Story source:</strong> Federation of American Societies for Experimental Biology</p><p>Journal References:</p><p>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</p>