Crohn's disease, a inflammatory bowel disease, affects the gastrointestinal tract. This disease has seen a sharp increase throughout much of Europe in recent decades. People suffering from this incurable condition have uncontrolled inflammation in their intestines, which leads to the formation of thickened and scarred connective tissue, or called fibrosis, and thus slows or blocks the movement of food. Patients usually need surgery to remove the scarred tissue in order to restore digestive function. Smokers with Crohn's 'more likely to suffer relapse after surgery. Now, researchers at the University of British Columbia have identified a genetic link that may improve the treatments for Crohn's patients. Described in Science Immunology, the study showed that a mutation prevented the development of fibrosis in a mouse model of Crohn's disease. The mutation did this by turning off a hormone receptor that induces immune response. The study was carried out on mice infected with a type of salmonella that imitates the symptoms caused by Crohn's disease. The researchers discovered that retinoic acid receptor–related orphan receptor α (RORα) and group 3 innate lymphoid cells (ILC3) contributed to the development of fibrosis. Mice deficient in RORα were protected from developing fibrosis. The findings could provide novel targets to reverse intestinal fibrosis caused by Crohn's disease. Fibrosis takes place due to an overproduction of proteins, witch harms the tissue function. Fibrosis occurs as a reparative response to injury or damage. The discoveries of this study might also apply to other fibrosis-related diseases. About RORα RORα, ne member of the retinoid orphan nuclear receptor (ROR) subfamily of orphan receptors, regulates inflammation, lipid metabolism, and cellular differentiation of several non-epithelial tissues. As a manufacturer, CusAb always offers high quality proteins like Recombinant CLDN6 and Biotin conjugated antibody for research at very attractive price.