EVIDENCE OF ENDOGENOUS REGULATORY FUNCTION OF TRANSFORMING GROWTH FACTOR-BETA-1 IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
EVIDENCE OF ENDOGENOUS REGULATORY FUNCTION OF TRANSFORMING GROWTH FACTOR-BETA-1 IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
复制标题
DOI：
10.1093/intimm/4.5.615
复制
发表时间：
1992-05-01
影响因子：
4.4
通讯作者：
MCFARLIN, DE
中科院分区：
文献类型：
--
作者：
RACKE, MK;CANNELLA, B;MCFARLIN, DE
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。已显示施用转化生长因子-β（TGF-β）抑制EAE。在这项研究中，内源性TGF-β在调节髓鞘碱性蛋白特异性T细胞系转移产生的复发性EAE中的可能作用进行了评估。虽然TGF-β不存在于正常的中枢神经系统中，但在急性和慢性疾病的中枢神经系统炎症区域中通过免疫组织学检测到这种细胞因子。在疾病发作时给予抗TGF-β导致EAE临床病程恶化和更广泛的病理学病变。这些发现为内源性TGF-β在慢性复发性EAE缓解中的作用提供了直接证据。
Experimental allergic encephalomyelitis (EAE) is an autoimmune disease characterized by inflammation and demyelination in the central nervous system (CNS). Administration of transforming growth factor-beta (TGF-beta) has been shown to inhibit EAE. In this study, the possible role of endogenous TGF-beta in the regulation of relapsing EAE produced by the transfer of myelin basic protein-specific T cell lines was assessed. Although TGF-beta is not present in the normal CNS, this cytokine was detected by immunohistology in areas of central nervous system inflammation in both acute and chronic disease. The administration of anti-TGF-beta at the disease onset led to a worsening of the clinical course of EAE and more extensive pathological lesions. These findings provide direct evidence for a role of endogenous TGF-beta in the remissions seen in chronic relapsing EAE.