Update on macrophages and innate immunity in scleroderma.
Update on macrophages and innate immunity in scleroderma.
复制标题
硬皮病中巨噬细胞和先天免疫的更新。
DOI：
10.1097/bor.0000000000000218
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发表时间：
2015-11
影响因子：
5.1
通讯作者：
Lu TT
中科院分区：
文献类型：
--
作者：
Chia JJ;Lu TT
在这篇2014年至2015年中期的文献综述中，我们研究了新的数据，揭示了巨噬细胞和其他先天免疫细胞和信号如何促进硬皮病的炎症、血管功能障碍和纤维化。最近的人体研究主要集中在硬皮病早期的变化，以及巨噬细胞与皮肤炎症和肺部疾病进展的联系。浆细胞样dc与血管功能障碍有关。在小鼠中，已经确定了影响巨噬细胞活化和实验性纤维化的几个因素。然而，新出现的数据也表明骨髓细胞在纤维化中有不同的作用。通过不同tlr的持续信号传导可导致炎症或纤维化，这些信号可影响免疫和非免疫细胞。有许多类型的先天免疫细胞可能对硬皮病有潜在的贡献，值得详细探索。通过实验剖析巨噬细胞在个体发生和激活状态中的作用，以及组织微环境中的先天信号通路，也可能有助于更好地理解硬皮病的发病机制。
In this review of the literature from 2014 through mid-2015, we examine new data that sheds light on how macrophages and other innate immune cells and signals contribute to inflammation, vascular dysfunction and fibrosis in scleroderma. Recent human studies have focused on changes early in scleroderma, and linked macrophages to inflammation in skin and progression of lung disease. Plasmacytoid DCs have been implicated in vascular dysfunction. In mice, several factors have been identified that influence macrophage activation and experimental fibrosis. However, emerging data also suggests that myeloid cells can have differential effects in fibrosis. Sustained signaling through different TLRs can lead to inflammation or fibrosis, and these signals can influence both immune and non-immune cells. There are many types of innate immune cells that can potentially contribute to scleroderma and will be worth exploring in detail. Experimentally dissecting the roles of macrophages based on ontogeny and activation state, and the innate signaling pathways in the tissue microenvironment, may also lead to better understanding of scleroderma pathogenesis.