Studies from Dr. Mari Shinohara are revealing how differences in the intensity of inflammation and innate immune system activation can drive different forms of disease in Experimental Autoimmune Encephalomyelitis (EAE), a mouse model of Multiple Sclerosis (MS). One form of the disease, elicited by relatively mild inflammatory stimuli, depends on inflammasome activity in innate immune cells, and can be successfully treated with interferon-beta. A more progressive and debilitating form of the disease can be elicited by more potent inflammatory stimuli, including viral infection. This disease cannot be treated with interferon-b, but does respond to treatments which block another inflammatory pathway defined by the beta lymphotoxin-b receptor and chemokine receptor CXCR2. This work, recently published in Nature Neuroscience, may have important implications for management of MS in humans, because it too is a heterogeneous disease, and only some patients respond to interferon-beta therapy.
Read the news release from DukeTODAY.