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Publication : SR-B1 Is a Silica Receptor that Mediates Canonical Inflammasome Activation.

First Author  Tsugita M Year  2017
Journal  Cell Rep Volume  18
Issue  5 Pages  1298-1311
PubMed ID  28147282 Mgi Jnum  J:251436
Mgi Id  MGI:6103837 Doi  10.1016/j.celrep.2017.01.004
Citation  Tsugita M, et al. (2017) SR-B1 Is a Silica Receptor that Mediates Canonical Inflammasome Activation. Cell Rep 18(5):1298-1311
abstractText  The inhalation of silica dust is associated with fibrosis and lung cancer, which are triggered by macrophage inflammatory responses; however, how macrophages recognize silica remains largely unknown. Here, we identify by functional expression cloning the class B scavenger receptor SR-B1 as a silica receptor. Through an extracellular alpha-helix, both mouse and human SR-B1 specifically recognized amorphous and crystalline silica, but not titanium dioxide nanoparticles, latex nanoparticles, or monosodium urate crystals, although all particles exhibited negative surface potentials. Genetic deletion of SR-B1 and masking of SR-B1 by monoclonal antibodies showed that SR-B1-mediated recognition of silica is associated with caspase-1-mediated inflammatory responses in mouse macrophages and human peripheral blood monocytes. Furthermore, SR-B1 was involved in silica-induced pulmonary inflammation in mice. These results indicate that SR-B1 is a silica receptor associated with canonical inflammasome activation.
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