Kupffer cell receptor CLEC4F is important for the destruction of desialylated platelets in mice.
Kupffer cell receptor CLEC4F is important for the destruction of desialylated platelets in mice.
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DOI：
10.1038/s41418-021-00797-w
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发表时间：
2021-11
影响因子：
12.4
通讯作者：
Xia L
中科院分区：
文献类型：
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作者：
Jiang Y;Tang Y;Hoover C;Kondo Y;Huang D;Restagno D;Shao B;Gao L;Michael McDaniel J;Zhou M;Silasi-Mansat R;McGee S;Jiang M;Bai X;Lupu F;Ruan C;Marth JD;Wu D;Han Y;Xia L
The liver has recently been identified as a major organ for destruction of desialylated platelets. However, the underlying mechanism remains unclear. Kupffer cells, which are professional phagocytic cells in the liver, comprise the largest population of resident tissue macrophages in the body. Kupffer cells express a C-type lectin receptor, CLEC4F, that recognizes desialylated glycans with an unclear in vivo role in mediating platelet destruction. In this study, we generated a CLEC4F-deficient mouse model (Clec4f−/−) and found that CLEC4F was specifically expressed by Kupffer cells. Using the Clec4f−/− mice and a newly generated platelet-specific reporter mouse line, we revealed a critical role for CLEC4F on Kupffer cells in mediating destruction of desialylated platelets in the liver in vivo. Platelet clearance experiments and ultrastructural analysis revealed that desialylated platelets were phagocytized predominantly by Kupffer cells in a CLEC4F-dependent manner in mice. Collectively, these findings identify CLEC4F as a Kupffer cell receptor important for the destruction of desialylated platelets induced by bacteria-derived neuraminidases, which provide new insights into the pathogenesis of thrombocytopenia in disease conditions such as sepsis.
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影响因子：
3.2
作者：
Grozovsky R;Giannini S;Falet H;Hoffmeister KM
通讯作者：
Hoffmeister KM
影响因子：
10.1
作者：
Marini I;Zlamal J;Faul C;Holzer U;Hammer S;Pelzl L;Bethge W;Althaus K;Bakchoul T
通讯作者：
Bakchoul T
影响因子：
16.6
作者：
Li J;van der Wal DE;Zhu G;Xu M;Yougbare I;Ma L;Vadasz B;Carrim N;Grozovsky R;Ruan M;Zhu L;Zeng Q;Tao L;Zhai ZM;Peng J;Hou M;Leytin V;Freedman J;Hoffmeister KM;Ni H
通讯作者：
Ni H
肝凝集素受体的双重作用在冷冻血小板的清除率中。
影响因子：
82.9
作者：
通讯作者：
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影响因子：
82.9
作者：
通讯作者：
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