Ulcerative Colitis Resource Center
Ulcerative Colitis Resource Center
November 22, 2017
1 min read

NIH funds research on exactly how TNF drives IBD

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The National Institute of Diabetes and Digestive and Kidney Diseases of the NIH has provided $1.5 million to fund research to determine exactly how the cell signaling protein tumor necrosis factor contributes to inflammatory bowel disease.

As the exact causes of IBD remain unknown, this research, led by Brent Polk, MD, AGAF, a pediatric gastroenterologist at the Children’s Hospital Los Angeles, and professor of pediatrics and biochemistry and molecular medicine at the Keck School of Medicine of University of Southern California, will explore how IBD is triggered on the cellular and molecular level, which could lead to new therapies for the disease, according to a press release.

The discovery that tumor necrosis factor (TNF) plays a central role in IBD led to the development of anti-TNF therapies, which many patients now use to manage their disease. However, many patients do not respond or lose response within a year of starting treatment, per the press release.

“Our goal is to better understand the cellular activity behind the mechanisms that drive injury or impair the normal repair responses to develop more precise treatment options for patients with IBD,” Polk said in the press release.

Although TNF is understood to promote inflammation, Polk and colleagues previously showed that it can also provide beneficial and protective effects on the intestine.

“The molecule TNF, which is part of a major signaling center in the body, actually has two different receptors, TNFR1 and TNFR2, which can be targeted to promote or reduce inflammation,” according to the press release. “The team established that TNFR2 drives a specific pathway that restricts inflammation.”

They are now researching how TNFR2 restricts the ability of immune cells to promote inflammation in the intestine, to try to understand exactly how it works to reduce inflammation.

Additionally, they are studying how TNFR2 causes intestinal stem cells to multiply or increase their response to repair intestinal injury in patients with IBD.
“By looking at how TNFR2 functions in both immune cells and in intestinal stem cells to reduce inflammation, we may be able to design new therapies that mimic the way the body does this naturally, and promote better health outcomes for our patients through a new precision medicine pathway” Polk said in the press release.

Disclosures: Healio Gastroenterology and Liver Disease was unable to determine Polk’s relevant financial disclosures at the time of publication.