Upregulation of thrombospondin-1(TSP-1) and its binding partners, CD36 and CD47, in sporadic inclusion body myositis

被引：18
|
作者：
Salajegheh, Mohammad
Raju, Raghavan
Schmidt, Jens
Dalakas, Marinos C.
机构：
[1] Brigham & Womens Hosp, Div Neuromusc Dis, Dept Neurol, Boston, MA 02115 USA
[2] Ctr Surg Res, Dept Surg, Birmingham, AL 35294 USA
[3] Univ Gottingen, Inst Expt & Clin, Muscle Immunobiol Sect, D-37073 Gottingen, Germany
[4] NINDS, Neuromusc Dis Sect, NIH, Bethesda, MD 20892 USA
来源：
JOURNAL OF NEUROIMMUNOLOGY | 2007年 / 187卷 / 1-2期
关键词：
inclusion body myositis; dermatomyositis; thrombospondin; CD47; CD36; amyloid;
D O I：
10.1016/j.jneuroim.2007.04.022
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
The TSPI/CD36/CD47-complex is involved in T cell expansion and inflammatory responses to beta-amyloid, both relevant to IBM. We report on the mRNA and protein expression of TSP1/CD36/CD47-complex in IBM muscles and in human myoblasts after cytokine stimulation. The TSP1/CD36/CD47 was upregulated in IBM. TSPI immunolocalized to the connective tissue contiguous to inflammation and CD36/CD47 on the myofibers and CD8+ cells. Further, TNF-alpha upregulated the production of TSP1 and CD47 by myoblasts. The TSP-complex is another inflammatory mediator associated with chronic inflammation in IBM that may perpetuate the immune responses to local antigens in response to TNF-alpha. (c) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码：166 / 174
页数：9
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