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Cyclodextrin-Mediated Cholesterol Depletion Induces Adiponectin Secretion in 3T3-L1 Adipocytes
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Concordance of Increased B1 Cell Subset and Lupus Phenotypes in Mice and Humans Is Dependent on BLK Expression Levels
AbstractPolymorphisms in the B lymphoid tyrosine kinase (BLK) gene have been associated with autoimmune diseases, including systemic lupus erythematosus, with risk correlating with reduced expression of BLK. How reduced expression of BLK causes autoimmunity is unknown. Using Blk+/+, Blk+/?, and Blk?/? mice, we show that aged female Blk+/? and Blk?/? mice produced higher anti-dsDNA IgG Abs and developed immune complex–mediated glomerulonephritis, compared with Blk+/+ mice. Starting at young age, Blk+/?
BANK1 Controls IgG Production Through TLR7-Dependent STAT1 Activation in a Lupus Model
The purpose of our study was to investigate the effects of the adaptor Bank1 in TLR7 signaling using the B6.Sle1.yaa mouse, a lupus model that develops disease through exacerbated TLR7 expression. Crosses of B6.Sle1.yaa with Bank1−/−mice maintained several B and myeloid cell phenotypes close to normal levels in wild-type mice. Most striking was the reduction in total serum IgG antibodies, but not of IgM, and reduced serum levels of autoantibodies, IL-6, and BAFF.
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