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A role of macrophage complement receptor CRIg in immune clearance and inflammation
Affiliation:1. Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA;2. Department of Protein Engineering, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA;1. Core Research Laboratory, The Second Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, China;2. Medical Research Council (MRC) Centre for Transplantation, King''s College London, Guy''s Hospital, London, UK;3. The Fifth Hospital of Xi’an, China;4. Department of General Surgery, The Second Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, China;1. Division of Hygiene and Medical Microbiology, Medical University of Innsbruck, Innsbruck, Austria;2. Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden;3. Linnæus Center of Biomaterials Chemistry, Linnæus University, SE-391 82 Kalmar, Sweden;1. Department of Immunology, Eötvös Loránd University, Pázmány P. s. 1/C, Budapest H-1117, Hungary;2. MTA-ELTE Immunology Research Group, Eötvös Loránd University, Pázmány P. s. 1/C, Budapest, H-1117, Hungary;1. Department of Immunology, ELTE Eötvös Loránd University, Budapest, Hungary;2. MTA-ELTE Complement Research Group, Department of Immunology, ELTE Eötvös Loránd University, Budapest, Hungary;1. Department of Microbiology and Immunology, Innovative Therapeutics Research Institute, Inje University College of Medicine, Republic of Korea;2. Department of Obstetrics and Gynecology, Republic of Korea;3. Paik Institute for Clinical Research, Busan, Republic of Korea;4. Department of Immunology, Oslo University Hospital, Oslo, Norway
Abstract:Complement receptor of the immunoglobulin superfamily (CRIg), also referred to as Z39Ig and V-set and Ig domain-containing 4 (VSIG4), has recently been implicated in the clearance of systemic pathogens and autologous cells. CRIg is exclusively expressed on tissue resident macrophages and binds to multimers of C3b and iC3b that are covalently attached to particle surfaces. Next to functioning as an important clearance receptor, CRIg's extracellular domain inhibits complement activation through the alternative, but not the classical, pathway, providing a novel tool to selectively block this pathway in vivo. Here, we review a role for CRIg in immune clearance, T-cell responses and complement regulation, and discuss the implications for disease manifestation.
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