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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Intravenous tolerance modulates macrophage classical activation and antigen presentation in experimental autoimmune encephalomyelitis.
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Intravenous tolerance modulates macrophage classical activation and antigen presentation in experimental autoimmune encephalomyelitis.

机译：在实验性自身免疫性脑脊髓炎中，静脉耐受可调节巨噬细胞经典激活和抗原呈递。

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Macrophages act as the first line of self defense by mounting an inflammatory response to antigen and as antigen presenting cells to initiate the adaptive immune response. Inhibition of macrophage activation is one of the possible approaches to modulate inflammation. Intravenous (i.v.) tolerance has proved to be an effective method for ameliorating experimental autoimmune diseases. Whether macrophages are involved in tolerance induction is still largely undefined. In the present study we found that i.v. tolerance induction resulted in lower B7.1, B7.2 and MHC class II molecules, and reduced phagocytosis by both peritoneal macrophages and adherent splenocytes. Macrophages from tolerized mice were associated with a significantly impaired response of MOG-sensitized T cells to MOG. Macrophages from tolerized mice produced low levels of pro-inflammatory molecules IL-12, TNF-alpha, IL-1beta, RANTES and MCP-1 and high levels of IL-10 and TGF-beta. Administration of anti-TGF-beta led to a reduction of IL-10 in tolerized mice. Thus, i.v. tolerance inhibits macrophage classical activation and APC function, increases macrophage alternative activation and IL-10 and TGF-beta production. These cytokines, in turn, induce enhanced production of IL-10 in macrophages in MOG i.v. mice.
机译：巨噬细胞通过对抗原发炎，并作为抗原呈递细胞来启动适应性免疫反应，从而充当了自我防御的第一线。抑制巨噬细胞活化是调节炎症的可能方法之一。静脉（i.v.）耐受已被证明是改善实验性自身免疫性疾病的有效方法。巨噬细胞是否参与耐受性的诱导仍然很大程度上不确定。在本研究中，我们发现耐受诱导导致较低的B7.1，B7.2和MHC II类分子，并减少了腹膜巨噬细胞和粘附的脾细胞的吞噬作用。来自耐受小鼠的巨噬细胞与MOG敏感的T细胞对MOG的反应显着受损有关。来自耐受小鼠的巨噬细胞产生低水平的促炎分子IL-12，TNF-α，IL-1β，RANTES和MCP-1，以及高水平的IL-10和TGF-β。抗TGF-β的给予导致耐受的小鼠中IL-10的降低。因此，i.v。耐受性抑制巨噬细胞经典激活和APC功能，增加巨噬细胞替代激活以及IL-10和TGF-β的产生。这些细胞因子继而在MOG i.v.中诱导巨噬细胞中IL-10的产生增加。老鼠。

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