Walker Margaret E, Hatfield Julianne K, Brown Melissa A
Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Avenue, Tarry 6-701, Chicago, IL 60611, USA.
Biochim Biophys Acta. 2012 Jan;1822(1):57-65. doi: 10.1016/j.bbadis.2011.02.009. Epub 2011 Feb 25.
Mast cells are classically considered innate immune cells that act as first responders in many microbial infections and have long been appreciated as potent contributors to allergic reactions. However, recent advances in the realm of autoimmunity have made it clear that these cells are also involved in the pathogenic responses that exacerbate disease. In the murine models of multiple sclerosis, rheumatoid arthritis and bullous pemphigoid, both the pathogenic role of mast cells and some of their mechanisms of action are shared. Similar to their role in infection and a subset of allergic responses, mast cells are required for the efficient recruitment of neutrophils to sites of inflammation. Although this mast cell-dependent neutrophil response is protective in infection settings, it is postulated that neutrophils promote local vascular permeability and facilitate the entry of inflammatory cells that enhance tissue destruction at target sites. However, there is still much to learn. There is little information regarding mechanisms of mast cell activation in disease. Nor is it known how many mast cell-derived mediators are relevant and whether interactions with other cells are implicated in these diseases including T cells, B cells and astrocytes. Here we review the current state of knowledge about mast cells in autoimmune disease. We also discuss findings regarding newly discovered mast cell actions and factors that modulate mast cell function. We speculate that much of this new information will ultimately contribute to a greater understanding of the full range of mast cell actions in autoimmunity. This article is part of a Special Issue entitled: Mast cells in inflammation.
肥大细胞传统上被认为是先天性免疫细胞，在许多微生物感染中作为第一反应者发挥作用，长期以来一直被视为过敏反应的重要促成因素。然而，自身免疫领域的最新进展表明，这些细胞也参与了加剧疾病的致病反应。在多发性硬化症、类风湿性关节炎和大疱性类天疱疮的小鼠模型中，肥大细胞的致病作用及其一些作用机制是相同的。与它们在感染和一部分过敏反应中的作用类似，肥大细胞是将中性粒细胞有效募集到炎症部位所必需的。虽然这种依赖肥大细胞的中性粒细胞反应在感染情况下具有保护作用，但据推测，中性粒细胞会促进局部血管通透性，并促进炎症细胞进入，从而增强靶部位的组织破坏。然而，仍有许多有待了解的地方。关于疾病中肥大细胞激活机制的信息很少。也不清楚有多少肥大细胞衍生的介质是相关的，以及与其他细胞的相互作用是否与包括T细胞、B细胞和星形胶质细胞在内的这些疾病有关。在这里，我们综述了自身免疫性疾病中肥大细胞的当前知识状态。我们还讨论了关于新发现的肥大细胞作用和调节肥大细胞功能的因素的研究结果。我们推测，这些新信息中的许多最终将有助于更全面地了解肥大细胞在自身免疫中的全部作用。本文是名为：炎症中的肥大细胞的特刊的一部分。
