Predicting Anti-TNF-Therapy Responsiveness

Research reveals a defect in myosin binding to TNFR2-M196R causes TNF-independent proinflammatory activity. The ability to genotype this polymorphism should help to predict inadequate responders to anti-TNF therapies early on, and allowing a personalized approach to the treatment of rheumatoid and psoriatic diseases.

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Targeting Tumor Necrosis Factor Pathways in Psoriatic Diseases: The Next Step

Preclinical models suggest that specific blockade of TNFR2 may significantly reduce inflammation and ameliorate signs of psoriatic diseases, while maintaining normal immune response in the host, including the ability to combat infection and cancer. In this article, M. Elaine Husni, MD, MPH, highlights her latest research and discusses her plans to use her new R01 grant to continue her translational work.

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