Estrogen inhibits systemic T cell expression of TNF-α and recruitment of TNF-α+ T cells and macrophages into the CNS of mice developing experimental encephalomyelitis
Estrogen inhibits systemic T cell expression of TNF-α and recruitment of TNF-α+ T cells and macrophages into the CNS of mice developing experimental encephalomyelitis
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DOI：
10.1006/clim.2001.5175
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发表时间：
2002-03-01
影响因子：
8.6
通讯作者：
Offner, H
中科院分区：
文献类型：
--
作者：
Ito, A;Buenafe, AC;Offner, H
已发现雌激素治疗在几种自身免疫模型中具有抑制活性。为了研究17 β-雌二醇（E2）抑制实验性自身免疫性脑脊髓炎的机制，我们评价了E2对MOG 35-55/CFA免疫的C57 BL/6小鼠中枢神经系统（CNS）和脾脏中TNF-α表达的影响。动力学分析表明，E2治疗大大减少了疾病发作时总炎症细胞以及TNF-α（+）巨噬细胞和T细胞向CNS的募集。相反，E2对驻留CNS小胶质细胞的相对高的组成型TNF-α表达仅具有中等影响。E2处理对脾CD 4（+）T细胞表达TNF-α也有显著的抑制作用，包括那些对MOG 35-55肽有反应的细胞。我们认为E2的保护机制可能涉及TNF-α表达的全身抑制和局部（CNS）炎症细胞的募集，对驻留CNS小胶质细胞的TNF-α表达有适度的影响。(C)2002年爱思唯尔科学（美国）。
Estrogen treatment has been found to have suppressive activity in several models of autoimmunity. To investigate the mechanism of 17beta-estradiol (E2) suppression of experimental autoimmune encephalomyelitis, we evaluated E2 effects on TNF-alpha expression in the central nervous system (CNS) and spleen of C57BL/6 mice immunized with MOG 35-55/CFA. Kinetic analysis demonstrated that E2 treatment drastically decreased the recruitment of total inflammatory cells as well as TNF-alpha(+) macrophages and T cells into the CNS at disease onset. In contrast, E2 had only moderate effects on the relatively high constitutive TNF-alpha expression by resident CNS microglial cells. E2 treatment also had profound inhibitory effects on expression of TNF-alpha by splenic CD4(+) T cells, including those responsive to MOG 35-55 peptide. We propose that the mechanism of E2 protection may involve both systemic inhibition of TNF-alpha expression and local (CNS) recruitment of inflammatory cells, with modest effects on TNF-alpha expression by resident CNS microglial cells. (C) 2002 Elsevier Science (USA).