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.
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To examine the possibility that anti-serpin B13 antibody affects non-inflamed islets in alternative ways that are independent of the effects on autoimmunity we injected healthy Balb/c animals with serpin B13 mAb and discovered that these mice had increased numbers of pancreatic islets, increased beta cell mass and β cell proliferation, and upregulated expression of Reg genes that have been implicated in β cell renewal.
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Our early studies in children with recent onset T1D revealed that patients with autoantibody to serpin B13 autoantibody maintain higher c-peptide levels during the first year postdiagnosis compared with those that are negative for this autoantibody.
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