Still, they are not perfect.
"The problem with that treatment is it is not effective against all autoimmune diseases," he said. "But more importantly, it may predispose to infection, because you downgrade the entire inflammatory response."
Siegel, with colleagues at the U.S. National Institute of Allergy and Infectious Diseases and at Cardiff University in Wales, U.K., asked what would happen to mouse models of asthma and multiple sclerosis that were genetically engineered to lack DR3. (Asthma is an inflammatory condition largely attributed to a subset of T-cells called Th2; multiple sclerosis is an autoimmune disorder caused by two different T-cell populations, Th1 and Th17.)
The answer: Both disease pathologies were "reduced" in the DR3-deficient mice, said Siegel, and fewer T-cells were found in the tissues that should have been affected. Yet, the DR3-deficient animals did not suffer from a generalized immunodeficiency and thus were able to mount immune responses to both a chicken egg protein and the parasite that causes toxoplasmosis.
"The essence of the paper is that not only are DR3-deficient mice not horribly immunodeficient," said Siegel, "if you look at their immune system in general, it is normal."
Indeed, the animals appeared to have no shortage of T-cells capable of responding to the inflammation-inducing antigens. Instead, for whatever reason, they were not being activated and dividing in the tissues normally affected by disease (such as the lung in the asthma model).
"It looks as if, for reasons this article does not make clear, the cells do not proliferate in the target organ," said Rose. "They can proliferate elsewhere, but they do not elicit an inflammatory response in the target organ."
Siegel said the combination of anti-inflammatory activity in DR3-deficient mice with sustained immune system function is u
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