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Autoimmune diseases are frustrating conditions in which the body's tissues are attacked by the "friendly fire" of its own protective immune system. Suppressing the immune system can be one way to treat autoimmune diseases but according to scientists from The Johns Hopkins University School of Medicine a new study shows that such blanket defenses are not the best. "In treating autoimmune disease," says Noel Rose, M.D., Ph.D., a professor of pathology at Hopkins, "it's possible that treatments that alter the immune system's overall function could make one autoimmune disease better but make a second one worse."

Treating these diseases can be frustrating because conditions that rise from the ashes of another are frequently seen. These are considered "opportunistic diseases". Scientists emphasize that different autoimmune diseases likely have different "good" and "bad" soldiers. For example, even though Interferon-gamma is protective in myocarditis, interferon-gamma is known to make multiple sclerosis worse. Dr. Rose adds that many autoimmune diseases are poorly understood, such as those linked to viral infections.

Immune-suppression may stop or lessen signs and symptoms but it actually predisposes the patient to more complications like cancer or bacterial overgrowth. Suppressing an autoimmune condition is like getting a mild case of AIDS. When the initial infections or other root causes are not dealt with, more and more damage continues to the body. Meanwhile other low grade problems begin making the disease process more difficult to control. Testing for the underlying root cause, developing a priority of treatment, and avoiding symptom suppression are three key elements experienced Practitioners like Dr. Peterson and Dr. Hecker can offer to patients with autoimmune diseases.

Marina Afanasyeva, Yan Wang, Ziya Kaya, Elizabeth A. Stafford, K. Malte Dohmen, Amir A. Sadighi Akha, and Noel R. Rose. Interleukin-12 Receptor/STAT4 Signaling Is Required for the Development of Autoimmune Myocarditis in Mice by an Interferon-?-Independent Pathway. Circulation. 2001;104:3145-3151