A new way for drugs proposed by researchers was found to be more effective against inflammatory bowel disease (IBD).
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‘IBD, a chronic inflammatory disease of the intestine, includes Crohn's disease and ulcerative colitis. It is commonly treated with one of several available biological drugs that block an inflammatory molecule called Tumor Necrosis Factor Alpha, or TNF-alpha, from binding to two receptors, TNFR1 and TNFR2. Only about 50 percent of patients are helped long term by this treatment.’
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"It is why it is targeted by drugs. Our interest in this study was to look for a more targeted therapy that might have a better impact than the existing approach, which is to block all TNF-alpha," Lo added. ![twitter](https://images.medindia.net/icons/news/social/twitter.png)
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The researcher explained that people have two different receptors, TNFR1 and TNFR2, in each of their cells that bind TNF-alpha. Currently, TNF-alpha-targeted drugs block both TNFR1 and TNFR2.
Lo’s experiments were done in mice, which have the same two receptors. The pattern of inflammation in mice is similar to that seen in humans.
TNF-alpha, produced by the body’s cells, also induces specialized immune and other cells, which both promote inflammation and suppress it. Thus, TNF-alpha plays a role in the destruction and the healing of tissues, a double-edged sword.
Lo said evidence exists that TNFR1 may be driving most of the destructive effects of IBD, whereas TNFR2 may drive the healing and restorative effects.
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Lo’s group was encouraged by two pieces of evidence suggesting that targeting TNFR1 may be a more beneficial strategy.
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Mice treated with this reagent were found to benefit from it. The researchers also did genetic targeting of TNFR1 to reduce its signaling. The impact, they found, was dramatic.
"When we reduced TNFR1 signaling, the mice showed a significant benefit relative to mice who had the full level of TNFR1 signaling," Lo said.
"This approach may offer more opportunity to TNFR2 to contribute to the healing."
Source-IANS