"This is potentially a huge finding," said Rose. "Companies would salivate to have something like this."
Yet Rose also noted that drugs against DR3 or TL1A likely would only help against diseases for which inflammation is the primary problem. "In autoimmune diseases in which antibodies play a major role [such as hemolytic anemia and Graves' disease], this probably would not be useful," he said.
Further, Rose noted that, in general, inflammation serves a useful, healthy purpose, immunologically speaking, and dampening it down might have undesirable effects. For example, there might be diseases or infections that could thrive in the absence of DR3 signaling.
One such case is tuberculosis, which can become active in individuals treated with TNF receptor blockers. Siegel said he is now testing to see whether the immune response to TB, or any other kind of infection, is weaker in mice without DR3 than normal mice.
A pair of recent studies -- one from the University of Miami and the other from M.D. Anderson Cancer Center in Houston and Biogen Idec in Cambridge, Mass. -- separately established a role for DR3/TL1A in both asthma and multiple sclerosis. The current study establishes that, in fact, the molecules do play a role in both diseases, said Siegel.
For more on autoimmune disorders, visit MedlinePlus.
SOURCES: Richard M. Siegel, M.D., Ph.D., National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Md.; Noel R. Rose, M.D., Ph.D., professor of pathology and molecular microbiology and immunology, and director, Johns Hopkins Center for Autoimmune Disease Research, Bloomberg Schoo
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