Medicity Research Laboratory, University of Turku, Turku, Finland.
The National Doctoral Programme in Informational and Structural Biology (ISB), Turku, Finland.
Front Immunol. 2018 Feb 6;9:114. doi: 10.3389/fimmu.2018.00114. eCollection 2018.
The injection of mannan into mice can result in the development of psoriasis (Ps) and psoriatic arthritis (PsA), whereas co-injection with antibodies toward collagen type II leads to a chronic rheumatoid-like arthritis. The critical event in all these diseases is mannan-mediated activation of macrophages, causing more severe disease if the macrophages are deficient in neutrophil cytosolic factor 1 (Ncf1), i.e., lack the capacity to make a reactive oxygen species (ROS) burst. In this study, we investigated the role of one of the receptors binding mannan; the macrophage mannose receptor (MR, CD206). MR is a C-type lectin present on myeloid cells and lymphatics. We found that mice deficient in MR expression had more severe mannan-induced Ps, PsA as well as rheumatoid-like arthritis. Interestingly, the MR-mediated protection was partly lost in mutated mice and was associated with an type 2 macrophage expansion. In conclusion, these results show that MR protects against a pathogenic inflammatory macrophage response induced by mannan and is associated with induction of ROS.
甘露聚糖注射到老鼠体内会导致银屑病（Ps）和银屑病关节炎（PsA）的发展，而与 II 型胶原抗体共同注射则会导致慢性类风湿样关节炎。在所有这些疾病中，关键事件是甘露聚糖介导的巨噬细胞激活，如果巨噬细胞缺乏中性粒细胞胞质因子 1（Ncf1），即缺乏产生活性氧（ROS）爆发的能力，则会导致更严重的疾病。在这项研究中，我们研究了结合甘露聚糖的受体之一的作用；巨噬细胞甘露聚糖受体（MR，CD206）。MR 是一种存在于髓样细胞和淋巴管上的 C 型凝集素。我们发现，MR 表达缺失的小鼠体内甘露聚糖诱导的 Ps、PsA 以及类风湿样关节炎更为严重。有趣的是，在 突变小鼠中，MR 介导的保护作用部分丧失，并且与 2 型巨噬细胞的扩张有关。总之，这些结果表明，MR 可防止甘露聚糖诱导的致病性炎症性巨噬细胞反应，并与 ROS 的诱导有关。
