Robbie-Ryan Michaela, Brown MelissaA
Graduate Program in Immunology and Molecular Pathogenesis, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Curr Opin Immunol. 2002 Dec;14(6):728-33. doi: 10.1016/s0952-7915(02)00394-1.
Two potential outcomes of dysregulated immunity are allergy and autoimmunity. Both are characterized by localized inflammation that leads to the injury and/or destruction of target tissues. Until recently, it was generally accepted that the mechanisms that govern these disease processes are quite disparate; however, new discoveries suggest that the mast cell may underlie much of the pathology in both these disease syndromes. Amongst these discoveries is the observation that mast cell-deficient mice exhibit significantly reduced disease severity compared to wild-type littermates in a murine model of multiple sclerosis (MS) and drugs that block mast cell function can improve clinical symptoms in this model. In addition, gene microarray analysis has revealed that the expression of several mast cell-specific genes is increased in the central nervous system plaques of MS patients. Although well established as effector cells in allergic inflammation, the location of mast cells and the wealth of inflammatory mediators they express make it likely that they have profound effects on many other autoimmune processes.
免疫调节失调的两个潜在后果是过敏和自身免疫。两者都以局部炎症为特征，这种炎症会导致靶组织的损伤和/或破坏。直到最近，人们普遍认为控制这些疾病过程的机制截然不同；然而，新的发现表明肥大细胞可能是这两种疾病综合征许多病理过程的基础。这些发现包括观察到在多发性硬化症（MS）小鼠模型中，与野生型同窝小鼠相比，肥大细胞缺陷小鼠的疾病严重程度显著降低，并且在该模型中阻断肥大细胞功能的药物可以改善临床症状。此外，基因微阵列分析显示，MS患者中枢神经系统斑块中几种肥大细胞特异性基因的表达增加。尽管肥大细胞作为变应性炎症中的效应细胞已得到充分证实，但其位置以及它们所表达的大量炎症介质表明它们可能对许多其他自身免疫过程产生深远影响。
