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URMC / Labs / Czyzyk Lab / Projects / Regulation of Pancreatic Islets Inflammation by Antibody Response to Serpin B13

Regulation of Pancreatic Islets Inflammation by Antibody Response to Serpin B13

Using a monoclonal antibody against serpin B13 as a model, we found that humoral activity against this serpin partially preserves the function of its protease targets and causes cleavage of the surface molecules CD4 and CD19 in lymphocytes that accumulate in the pancreatic islets in NOD mice with spontaneous autoimmune diabetes.  Consequently, T cell with the truncated form of CD4 secrete reduced levels of interferon-γ, a cytokine that has been implicated in the pathogenesis of type 1 diabetes.  This data suggests that anti-serpin activity prevents serpin molecules from neutralizing proteases, thereby impairing leukocyte function and reducing the severity of autoimmune inflammation.

Model of inhibition of islet inflammation

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