Toll-like receptor 2 mediates CNS injury in focal cerebral ischemia

被引：211

作者：

Lehnardt, Seija ^{[1
]}

Lehmann, Sabrina ^{[1
]}

Kaul, David ^{[1
]}

Tschimmel, Katharina ^{[1
]}

Hoffmann, Olaf ^{[1
]}

Cho, Sabine ^{[1
]}

Krueger, Christina ^{[1
]}

Nitsch, Robert ^{[1
]}

Meisel, Andreas ^{[1
]}

Weber, Joerg R. ^{[1
]}

机构：

[1] Charite Univ Med Berlin, Dept Expt Neurol, D-10117 Berlin, Germany

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2007年 / 190卷 / 1-2期

关键词：

stroke; focal cerebral ischemia; toll-like receptor; microglia;

D O I：

10.1016/j.jneuroim.2007.07.023

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Toll-like receptors (TLR) recognize molecular structures associated with pathogens as well as host-derived components and initiate an inflammatory innate immune response. Microglia represent the resident immune host defense and are the major inflammatory cell type in the central nervous system (CNS). We show here that TLR2-deficient mice develop a decreased CNS injury compared to wild type mice in a model of focal cerebral ischemia. TLR2 mRNA is up-regulated in wild type mice during cerebral ischemia. In ischemic brains, TLR2 protein is expressed in lesion-associated microglia. Absence of TLR2 does not affect the recruitment of granulocytes to the infarct region. We conclude that TLR2 in microglia propagates stroke-induced CNS injury. (C) 2007 Elsevier B.V. All rights reserved.

引用

页码：28 / 33

页数：6

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