Racke M K, Dhib-Jalbut S, Cannella B, Albert P S, Raine C S, McFarlin D E
Neuroimmunology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 30892.
J Immunol. 1991 May 1;146(9):3012-7.
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.
实验性变应性脑脊髓炎（EAE）是一种自身免疫性疾病，其特征为中枢神经系统的炎症和脱髓鞘。研究了免疫抑制分子转化生长因子-β（TGF-β1）对髓鞘碱性蛋白特异性T细胞系转移所产生的慢性复发性EAE的影响。TGF-β1在体外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，即使在疾病进展期间给予TGF-β1，其体内给药也始终能改善临床病程。免疫病理学研究表明，在TGF-β1治疗的小鼠中，中枢神经系统损伤以及细胞表面淋巴细胞功能相关抗原-1和II类MHC分子的表达显著减少。这些发现已将TGF-β1确定为人类脱髓鞘疾病多发性硬化症的一种可能治疗剂。
