19 Jan 17

In a previous study by other researchers, demonstrated an early stage clinical trial that IBD patients have improved if there is a monoclonal antibody, IL-23 and a related inflammatory mediators malegra . Moreover, recent studies demonstrated in mice in which the gene for IL – 23 is deleted, that IL – 23 development and maintenance of development and maintenance of chronic intestinal inflammation. Such evidence, the current the current discovery, suggests therapies targeting the IL-23 pathway to more individual and better directed therapies for IBDs can cause, the authors say. ‘This important discovery not only offers new hope for better treatments for people with Crohn’s disease, it also highlights the promise of the human genome project and subsequent investments by the NIH in large scale, collaborative research projects to hopefully the causes of unraveling, and for complex for complex, enigmatic diseases, ‘said Stephen P. Director, Division of digestive diseases and Nutrition at the National Institutes of Health NIDDK. Has offers a warning, ‘The IL-23 pathway may be a very useful purpose protects serve us against other diseases, the search the search or to manipulate their activity with drugs or other means, we need to consider this balancing act,’said them.

About 1 million Americans Crohn’s disease or colitis, collectively known as inflammatory bowel disease .The authors of the study represent the IBD Genetics Consortium, which National Institute of Diabetes National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health . Consortium member institutions are Cedars-Sinai Medical Center in Los Angeles, the University of Chicago, Johns Hopkins University, Universite de Montreal, the University of Pittsburgh, Mount Sinai Hospital in Toronto and the University of Toronto and Yale University.

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