Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1.

Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1.
复制标题

DOI:
10.4049/jimmunol.146.9.3012
复制
发表时间:
1991-05
影响因子:
4.4
通讯作者:
M. Racke;S. Dhib-Jalbut;B. Cannella;P. Albert;C. Raine;D. McFarlin
M. Racke;S. Dhib-Jalbut;B. Cannella;P. Albert;C. Raine;D. McFarlin
中科院分区:
医学2区
文献类型:
--
作者:
M. Racke;S. Dhib-Jalbut;B. Cannella;P. Albert;C. Raine;D. McFarlin

文献摘要

被引文献

相似文献

实验性变态反应性脑脊髓炎(EAE)是一种以中枢神经系统炎症和脱髓鞘为特征的自身免疫性疾病。研究了免疫抑制分子转化生长因子-β(TGF-β 1)对转移髓鞘碱性蛋白特异性T细胞系产生的慢性复发性EAE的影响。TGF-β 1在体外可显著抑制髓鞘碱性蛋白特异性淋巴结细胞的活化和增殖。这降低了这些细胞转移EAE的能力。此外,体内给予TGF-β 1始终导致临床病程改善,即使在疾病持续期间给予。免疫病理学研究表明,在TGF-β 1治疗的小鼠中枢神经系统损伤和细胞表面淋巴细胞功能相关的Ag-1和II类MHC分子的表达显着减少。这些发现已经确定TGF-β 1作为人类脱髓鞘疾病多发性硬化症的可能治疗剂。
Experimental allergic encephalomyelitis (EAE) is an autoimmune disease characterized by inflammation and demyelination in the central nervous system. The effect of the immunosuppressive molecule transforming growth factor-beta, (TGF-beta 1) on chronic relapsing EAE produced by the transfer of myelin basic protein-specific T cell lines was studied. TGF-beta 1 markedly inhibited the activation and proliferation of myelin-basic protein-specific lymph node cells in vitro. This reduced the capacity of these cells to transfer EAE. In addition, administration of TGF-beta 1 in vivo consistently resulted in an improved clinical course, even when given during ongoing disease. Immunopathologic study demonstrated a marked reduction in central nervous system damage and expression of cell-surface lymphocyte function-associated Ag-1 and class II MHC molecules in TGF-beta 1-treated mice. These findings have identified TGF-beta 1 as a possible therapeutic agent for the human demyelinating disease multiple sclerosis.