期刊
SCIENCE
卷 363, 期 6423, 页码 142-142出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aao5213
关键词
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资金
- NIH [T32 AR007108, T32 AI007044-39, T32 AI106677, R21 CA195256, R01 DK09369, R01 AI118803, R01 AI081948, R01 AI113325, R21 AI138067, R21 ES024437]
- AAI Fellowship
- NSF [DGE-0718124]
- DOD [BCRP W81XWH-08-1-0570]
- Lupus Research Alliance
Cytopenias are an important clinical problem associated with inflammatory disease and infection. We show that specialized phagocytes that internalize red blood cells develop in Toll-like receptor 7 (TLR7)-driven inflammation. TLR7 signaling caused the development of inflammatory hemophagocytes (iHPCs), which resemble splenic red pulp macrophages but are a distinct population derived from Ly6C(hi) monocytes. iHPCs were responsible for anemia and thrombocytopenia in TLR7-overexpressing mice, which have a macrophage activation syndrome (MAS)-like disease. Interferon regulatory factor 5 (IRF5), associated with MAS, participated in TLR7-driven iHPC differentiation. We also found iHPCs during experimental malarial anemia, in which they required endosomal TLR and MyD88 signaling for differentiation. Our findings uncover a mechanism by which TLR7 and TLR9 specify monocyte fate and identify a specialized population of phagocytes responsible for anemia and thrombocytopenia associated with inflammation and infection.
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