mmatory response, says Chen. Bcl-3 appears to take in information from the body and, in response to infection, interferes with p50 degradation to decrease inflammatory response.
Inflammation is natural, says Chen. If we didnt respond to infectious agents, bacteria would kill us. However, the inflammatory response must be controlled or we could also die. Bcl-3 helps regulate inflammation.
By using what we now know about Bcl-3 regulatory function, we hope to create new ways to control inflammation for therapeutic purposes with selective anti-inflammatory agents, says Carmody.
Although drugs to suppress inflammation currently exist, Chen and Carmody say they cause many undesirable side effects in patients with inflammatory diseases.
Current drug treatments target inflammation signaling pathways. When you inhibit entire pathways, you can produce negative side effects, said Carmody. Since Bcl-3 acts on specific genes, we should be able to target a subset of dangerous regulatory genes without disrupting other important immune responses. Such drugs could benefit patients with chronic inflammation and transplant recipients as well as those suffering with inflammatory diseases.
In the future, the scientists aim to determine the components of the cell responsible for flagging p50 for destruction and instructing Bcl-3 to perform its vital function.
Contact: Karen Kreeger
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