Monday, October 19, 2020

Researchers Identify Enzyme That Contributes To Development Of Lupus..

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Researchers at Beth Israel Deaconess Medical Center (BIDMC) have identified an enzyme that is significantly elevated in mouse models of systemic lupus erythematosus and in blood samples of patients with this disease.Published online in The Journal of Clinical Investigation, the new findings demonstrate that inhibition of the SHP-2 enzyme can significantly diminish lupus symptoms — including skin lesions, enlarged spleen and kidney failure — and suggest that development of a SHP-2 inhibitor drug could offer a new therapeutic approach for this often debilitating disease.Researchers at Beth Israel Deaconess Medical Center (BIDMC) have identified an enzyme that is significantly elevated in mouse models of systemic lupus erythematosus and in blood samples of patients with this diseas. Published online in The Journal of Clinical Investigation, the new findings demonstrate that inhibition of the SHP-2 enzyme can significantly diminish lupus symptoms — including skin lesions, enlarged spleen and kidney failure — and suggest that development of a SHP-2 inhibitor drug could offer a new therapeutic approach for this often debilitating disease.

Systemic lupus erythematosus is a chronic autoimmune disease that causes widespread inflammation and tissue damage to organ systems throughout the body. There is no cure for the disease, which primarily strikes young women in their 20s and 30s and affects an estimated 1.5 million individuals in the United States and at least 5 million worldwide.”SHP-2 can lead to an overproduction of cytokine molecules,” explained senior author Maria Kontaridis, PhD, Interim Director of the Basic Cardiology Research Program in the CardioVascular Institute at BIDMC and Assistant Professor of Medicine at Harvard Medical School (HMS). “In patients with lupus, we know that cytokines trigger inflammation, contribute to immune cell dysfunction, and lead to organ damage.”

Kontaridis, whose mother battled lupus for more than 25 years — has spent more than a decade studying genetic mutations in a class of enzymes known as protein tyrosine phosphatases. Her previous work has revealed that mutations in these proteins alter cellular signaling pathways, leading to the development of a group of rare congenital heart diseases known as RASopathies. Several years ago, after learning that more than 50 children with a RASopathy disorder called Noonan syndrome had also developed lupus, Kontaridis hypothesized that there might be a correlation between phosphatase activity and systemic autoimmunity.

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