Frontier Research Institute for Interdisciplinary Sciences, Tohoku University, Sendai, Japan.
PRESTO, Japan Science and Technology Agency, Kawaguchi, Japan.
Front Immunol. 2018 Jan 29;9:103. doi: 10.3389/fimmu.2018.00103. eCollection 2018.
Inhalation of exogenous crystals such as silica, asbestos, and carbon nanotubes can cause lung fibrosis and cancer. Endogenous crystals such as monosodium urate, cholesterol, and hydroxyapatite are associated with pathogenesis of gout, atherosclerosis, and osteoarthritis, respectively. These crystal-associated-inflammatory diseases are triggered by the macrophage NLRP3 inflammasome activation and cell death. Therefore, it is important to understand how macrophages recognize crystals. However, it is unlikely that macrophages have evolutionally acquired receptors specific for crystals or recently emerged nanoparticles. Several recent studies have reported that some crystal particles are negatively charged and are recognized by scavenger receptor family members in a charge-dependent manner. Alternatively, a model for receptor-independent phagocytosis of crystals has also been proposed. This review focuses on the mechanisms by which macrophages recognize crystals and nanoparticles.
吸入二氧化硅、石棉和碳纳米管等外源性晶体可引起肺纤维化和癌症。内源性晶体,如单钠尿酸盐、胆固醇和羟磷灰石,分别与痛风、动脉粥样硬化和骨关节炎的发病机制有关。这些晶体相关的炎症性疾病是由巨噬细胞 NLRP3 炎性体激活和细胞死亡引发的。因此,了解巨噬细胞如何识别晶体很重要。然而,巨噬细胞不太可能进化出专门识别晶体或最近出现的纳米颗粒的受体。最近的几项研究报告称,一些晶体颗粒带负电荷,并以电荷依赖的方式被清道夫受体家族成员识别。或者,也提出了一种晶体非受体依赖性吞噬的模型。这篇综述主要关注巨噬细胞识别晶体和纳米颗粒的机制。