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J Neuroimmunol. 2007 Jul;187(1-2):166-74. Epub 2007 Jun 18.

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

Author information

1
The Division of Neuromuscular Disease, Department of Neurology, Brigham and Women's Hospital, 75 Francis Street, Tower 5D, Boston, MA 02115, USA.

Abstract

The TSP1/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. TSP1 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.

PMID:
17572512
DOI:
10.1016/j.jneuroim.2007.04.022
[Indexed for MEDLINE]

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