Different pathological roles of toll-like receptor 9 on mucosal B cells and dendritic cells in murine IgA nephropathy.
Different pathological roles of toll-like receptor 9 on mucosal B cells and dendritic cells in murine IgA nephropathy.
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DOI：
10.1155/2011/819646
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发表时间：
2011
影响因子：
--
通讯作者：
Tomino Y
中科院分区：
文献类型：
--
作者：
Kajiyama T;Suzuki Y;Kihara M;Suzuki H;Horikoshi S;Tomino Y
伊加肾病（IgAN）的发病机制尚不清楚，但粘膜免疫在病理上的作用包括致肾炎性伊加和伊加免疫复合物（IC）的产生已被讨论。我们已经报道了粘膜Toll样受体（TLR）-9参与人和小鼠IgAN的发病机制。然而，粘膜中表达TLR 9的细胞类型仍不清楚。为了解决这一问题，我们将细胞特异性CpG DNA（（i）：树突状细胞：（DC），（ii）：B细胞，（iii）：两者）（称为TLR 9的配体）经鼻攻击IgAN易感小鼠，并分析每组的疾病表型。每周给药8次后，各组肾小球损害加重。CpG-A组肾小球系膜增生性病变明显扩大，血清IgA-IgG 2a IC和肾小球沉积增加; CpG-B组肾小球硬化性病变扩大，血清和肾小球伊加及M2巨噬细胞浸润增加。目前的结果表明，粘膜TLR 9对B细胞和DC可能不同地有助于这种疾病的进展，通过诱导肾炎伊加或IgA-IgG IC，分别。这张照片提示了儿童和成人IgAN之间的病理差异。
Although pathogenesis of IgA nephropathy (IgAN) is still obscure, pathological contribution of mucosal immunity including production of nephritogenic IgA and IgA immune complex (IC) has been discussed. We have reported that mucosal toll-like receptor (TLR)-9 is involved in the pathogenesis of human and murine IgAN. However, cell-type expressing TLR9 in mucosa remains unclear. To address this, we nasally challenged cell-specific CpG DNA ((i): dendritic cell: (DC), (ii): B cell, (iii): both), known as ligand for TLR9, to IgAN prone mice and analyzed disease phenotype of each group. After 8 times of the weekly administration, every group showed deterioration of glomerular damage. However, CpG-A-group showed clear extension of mesangial proliferative lesions with increase of serum IgA-IgG2a IC and its glomerular depositions, while CpG-B-group showed extent of glomerular sclerotic lesions with increase of serum and glomerular IgA and M2 macrophage infiltration. Present results indicate that mucosal TLR9 on B cells and DC may differently contribute to the progression of this disease via induction of nephritogenic IgA or IgA-IgG IC, respectively. This picture is suggestive for the pathological difference between child and adult IgAN.
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影响因子：
3.4
作者：
Harper, SJ;Allen, AC;Feehally, J
通讯作者：
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影响因子：
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19.6
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通讯作者：
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