| Literature DB >> 27477514 |
Efstathios G Stamatiades1, Marie-Eve Tremblay2, Mathieu Bohm3, Lucile Crozet4, Kanchan Bisht2, Daniela Kao5, Carolina Coelho1, Xiying Fan6, William T Yewdell1, Anne Davidson7, Peter S Heeger8, Sandra Diebold9, Falk Nimmerjahn5, Frederic Geissmann10.
Abstract
Small immune complexes cause type III hypersensitivity reactions that frequently result in tissue injury. The responsible mechanisms, however, remain unclear and differ depending on target organs. Here, we identify a kidney-specific anatomical and functional unit, formed by resident macrophages and peritubular capillary endothelial cells, which monitors the transport of proteins and particles ranging from 20 to 700 kDa or 10 to 200 nm into the kidney interstitium. Kidney-resident macrophages detect and scavenge circulating immune complexes "pumped" into the interstitium via trans-endothelial transport and trigger a FcγRIV-dependent inflammatory response and the recruitment of monocytes and neutrophils. In addition, FcγRIV and TLR pathways synergistically "super-activate" kidney macrophages when immune complexes contain a nucleic acid. These data identify a physiological function of tissue-resident kidney macrophages and a basic mechanism by which they initiate the inflammatory response to small immune complexes in the kidney.Entities:
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Year: 2016 PMID： 27477514 PMCID： PMC4983224 DOI： 10.1016/j.cell.2016.06.058
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582