Autoimmune disease such as myocarditis involves an excess of interleukin-12 (IL-12) generating subsequent production of interferon-gamma (IFN-γ). Non-specific immunosuppressive drugs are prescribed for the treatment of these conditions. But, in December 18 Circulation, Marina Afanasyeva and colleagues from Johns Hopkins University School of Medicine show that suppressing IFN-γ or the entire immune system is unlikely to be the best way to treat autoimmune disease.

Afanasyeva et al. studied IL-12 receptor signaling in the development of murine experimental autoimmune myocarditis (EAM) and found that IFN-γ helps prevent tissue damage in EAM. Lack of IFN-γ exacerbated myocarditis and the spleens of these mice had greater numbers of CD3+, CD4+, CD8+ and IL-2–producing cells. But treatment of mice with recombinant IFN-γ suppressed these effects and the development of myocarditis (Circulation 2001, 104:3145).

Noel Rose, Professor of Pathology at Johns Hopkins and senior author of the paper concluded that, "in treating...

Interested in reading more?

Become a Member of

Receive full access to more than 35 years of archives, as well as TS Digest, digital editions of The Scientist, feature stories, and much more!
Already a member?