B Cell Subsets Contribute to Renal Injury and Renal Protection after Ischemia/Reperfusion
作者： Brandon Renner , Derek Strassheim , Claudia R. Amura , Liudmila Kulik , Danica Ljubanovic
关键词: Ischemia 、 Immune system 、 B cell 、 Reperfusion injury 、 Classical complement pathway 、 Immunology 、 Endocrinology 、 Immunoglobulin M 、 Kidney 、 Biology 、 Internal medicine 、 Complement system
摘要: Ischemia/reperfusion (I/R) triggers a robust inflammatory response within the kidney. Numerous components of immune system contribute to resultant renal injury, including complement system. We sought identify whether natural Abs bind postischemic kidney and activation after I/R. depleted peritoneal B cells in mice by hypotonic shock. Depletion prevented deposition IgM glomeruli I/R attenuated injury found that glomerular activates classical pathway complement, but it does not cause substantial C3 Furthermore, deficient proteins were protected from indicating through pathway. also subjected all mature (μMT mice) they sustained worse than wild-type controls. Serum IL-10 levels lower μMT mice. Taken together, these results indicate Ab produced binds glomerulus contributes functional injury. However, nonperitoneal attenuate I/R, possibly production IL-10.
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