B细胞激活因子
系膜
免疫球蛋白A
固有层
生物
免疫系统
免疫学
抗体
生发中心
肾小球肾炎
肾病
肾炎
免疫球蛋白类转换
B细胞
内分泌学
肾
免疫球蛋白G
上皮
遗传学
糖尿病
作者
Douglas D. McCarthy,Sidney Chiu,Yunfei Gao,Leslie Summers-Deluca,Jennifer L. Gommerman
标识
DOI:10.1016/j.cellimm.2006.08.002
摘要
BAFF is a peripheral B cell survival factor and can mediate antibody (Ab) class switching. Over-expression of BAFF in mice results in B cell hyperplasia, elevated serum immunoglobulin (Ig), spontaneous germinal centre (GC) reactions and mild glomerulonephritis (GN). Here we show that, in addition to driving excessive levels of serum IgA, BAFF over-expression results in increased IgA levels within the intestinal lamina propria (LP) and deposition of IgA immune complexes in the renal glomerular mesangium. LIGHT has been previously shown to mediate a similar phenotype via signaling through the lymphotoxin-beta receptor (LTbetaR). We evaluated if LIGHT and BAFF cooperate in the etiology of a hyper-IgA syndrome in BAFF-overexpressing transgenic (BAFF-Tg) mice. We find that LIGHT-deficient BAFF-Tg mice exhibit similar levels of IgA in the serum, gut and kidney and develop nephritis to the same degree as LIGHT-sufficient BAFF-Tg mice. Therefore, in the context of BAFF over-expression, LIGHT is dispensable for the generation of a hyper-IgA syndrome accompanied by nephritis.
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