't Hart Bert A, Weissert Robert
Department of Immunobiology, Biomedical Primate Research Centre, The Netherlands.
Department of Neurology, University of Regensburg, Germany.
Mult Scler J Exp Transl Clin. 2016 Feb 7;2:2055217316630999. doi: 10.1177/2055217316630999. eCollection 2016 Jan-Dec.
Myelin oligodendrocyte glycoprotein (MOG) is a candidate primary target of the autoimmune attack on the central nervous system (CNS) in multiple sclerosis (MS). However, the physiological function of MOG has been unclear for a long time.
We propose that MOG has a central role in the regulation of tolerance and autoimmunity.
The interaction of MOG with DC-SIGN, an innate antigen receptor of myeloid antigen-presenting cells (m-APCs), present inside the CNS (microglia) or in draining lymph nodes (dendritic cells; DCs), keeps these cells in an immature/tolerogenic state. We postulate that this tolerogenic mechanism may be disturbed in MS by unknown factors.
髓鞘少突胶质细胞糖蛋白(MOG)是多发性硬化症(MS)中自身免疫攻击中枢神经系统(CNS)的主要候选靶点。然而,长期以来MOG的生理功能尚不清楚。
我们提出MOG在耐受性和自身免疫调节中起核心作用。
MOG与DC-SIGN相互作用,DC-SIGN是髓样抗原呈递细胞(m-APC)的一种天然抗原受体,存在于CNS内(小胶质细胞)或引流淋巴结(树突状细胞;DC)中,使这些细胞保持未成熟/耐受性状态。我们推测,这种耐受性机制在MS中可能会受到未知因素的干扰。