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Abnormal SHP2 signaling contributes to lupus-like symptoms in mice

JCI Journals

In systemic lupus erythematosus, inappropriate innate and adaptive immune responses lead to inflammation and organ damage, but it is not fully understood how this disease develops. Abnormalities in protein phosphatases, which regulate cellular activity, have been linked to several autoimmune conditions. Recent studies have shown that individuals with mutations in a protein phosphatase called SHP2 have a high risk of developing lupus. In this month's issue of the JCI, a research group led by Maria Kontaridis of Harvard University identifies a link between lupus and elevations in SHP2 activity. The authors discovered that SHP2 activity is elevated the spleens of mice with lupus-like symptoms compared to healthy mice. Moreover, lupus patients also had elevations in SHP2 activity in their blood cells relative to healthy patients. Inhibition of SHP2 signaling in the lupus-prone mice improved lupus-like symptoms, increased lifespan, and normalized inflammation. Targeting SHP2 in T cells isolated from lupus patients also reduced the production of inflammatory cytokines. This study suggests that abnormal SHP2 signaling contributes to lupus pathogenesis and indicates that pharmacologically targeting the SHP2 pathway may be an effective therapy for this disease.



Inhibition of SHP2 Ameliorates the Pathogenesis of Systemic Lupus Erythematosus


Maria Kontaridis
Beth Israel Deaconess Medical Center

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