Novel molecule stops and could reverse rheumatoid arthritis
A Northwestern University researcher has developed a novel molecule that can cause immune cells responsible for rheumatoid arthritis to self-destruct. The molecule, dubbed Casper the Ghost, is an imitation that can go undetected then penetrate overactive immune cells that proliferate in the blood of individuals with rheumatoid arthritis and cause rogue immune cells to commit suicide.
The molecule that could stop and even reverse rheumatoid arthritis was invented by a researcher from Northwestern University Feinberg School of Medicine. "This new therapy stopped the disease cold in 75 percent of the mice," reported Harris Perlman, the lead author and an associate professor of medicine at Feinberg. "The best part was we didn't see any toxicity. This has a lot of potential for creating an entirely new treatment for rheumatoid arthritis."
Immune cells that become active in rheumatoid arthritis do not die – something that normally occurs after bacteria and viruses are destroyed. Instead they float around where they continue to grow and deposit in joints that leads to pain, inflammation and destruction of cartilage and bone. There is no currently no non-toxic way to stop the immune cells that lead to rheumatoid arthritis from proliferating.
Dr. Perlman found that immune cells of individuals with rheumatoid arthritis are critically low in a key molecule called Bim that is crucial for “telling” rogue immune cells to self destruct. He invented an imitation molecule called BH3 mimetic that invaded immune cells called macrophages. When he injected BH3 mimetic in mice with rheumatoid arthritis, bone destruction and joint swelling decreased. BH3 destroyed the immune cells that cause rheumatoid arthritis.
The scientist hopes to develop a technique using nanotechnology to deliver the novel molecule as drug therapy to stop and even reverse rheumatoid arthritis. Current treatments for rheumatoid arthritis have major drawbacks because of side effects and lack of effectiveness.