Salajegheh Mohammad, Raju Raghavan, Schmidt Jens, Dalakas Marinos C
The Division of Neuromuscular Disease, Department of Neurology, Brigham and Women's Hospital, 75 Francis Street, Tower 5D, Boston, MA 02115, USA.
J Neuroimmunol. 2007 Jul;187(1-2):166-74. doi: 10.1016/j.jneuroim.2007.04.022. Epub 2007 Jun 18.
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.
TSP1/CD36/CD47复合物参与T细胞扩增以及对β-淀粉样蛋白的炎症反应,这两者均与包涵体肌炎(IBM)相关。我们报告了细胞因子刺激后,TSP1/CD36/CD47复合物在IBM肌肉和人成肌细胞中的mRNA和蛋白质表达情况。TSP1/CD36/CD47在IBM中上调。TSP1免疫定位于与炎症相邻的结缔组织以及肌纤维和CD8+细胞上的CD36/CD47。此外,肿瘤坏死因子-α(TNF-α)上调了成肌细胞中TSP1和CD47的产生。TSP复合物是与IBM慢性炎症相关的另一种炎症介质,它可能会使机体对局部抗原的免疫反应因TNF-α而持续存在。