Cutting edge:: TLR3 stimulation suppresses experimental autoimmune encephalomyelitis by inducing endogenous IFN-β
Cutting edge:: TLR3 stimulation suppresses experimental autoimmune encephalomyelitis by inducing endogenous IFN-β
复制标题
DOI：
10.4049/jimmunol.177.11.7505
复制
发表时间：
2006-12-01
影响因子：
4.4
通讯作者：
Gran, Bruno
中科院分区：
文献类型：
--
作者：
Touil, Tarik;Fitzgerald, Denise;Gran, Bruno
实验性自身免疫性脑脊髓炎是细胞介导的自身免疫的一种充分表征的模型。 APC 上表达的 TLR 可以识别微生物成分并诱导先天免疫反应，从而消除入侵的传染源。据报道，某些 TLR 激动剂对中枢神经系统自身免疫性炎症脱髓鞘具有辅助作用。我们在这项研究中报道，在小鼠实验性自身免疫性脑脊髓炎模型中，聚肌胞苷酸（一种双链 RATA 类似物）刺激 TLR3 可抑制复发性脱髓鞘。疾病抑制与内源性 IFN-β 的诱导和 CC 趋化因子 CCL2 的外周诱导有关。这些数据表明，优先激活不依赖于 MyD88 的 I 型 IFN 诱导 TLR 通路在这种器官特异性自身免疫性疾病中具有免疫调节潜力。免疫学杂志，2006 年，177：7505-7509。
Experimental autoimmune encepbalomyelitis is a well characterized model of cell-mediated autoimmunity. TLRs expressed on APCs recognize microbial components and induce innate immune responses, leading to the elimination of invading infectious agents. Certain TLR agonists have been reported to have adjuvant properties in CNS autoimmune inflammatory demyelination. We report in this study that TLR3 stimulation by polyinosinic polycytidylic acid, a double-stranded RATA analog, suppresses relapsing demyelination in a murine experimental autoimmune encepbalomyelitis model. Disease suppression is associated with the induction of endogenous IFN-beta and the peripheral induction of the CC chemokine CCL2. These data indicate that a preferential activation of the MyD88-independent, type I IFN-inducing TLR pathway has immunoregulatory potential in this organ-specific autoimmune disease. The Journal of Immunology, 2006, 177:7505-7509.