{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Macleod OJS"],"funding":["Medical Research Council","Wellcome Trust"],"pagination":["5085"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9424271"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["African trypanosomes are extracellular pathogens of mammals and are exposed to the adaptive and innate immune systems. Trypanosomes evade the adaptive immune response through antigenic variation, but little is known about how they interact with components of the innate immune response, including complement. Here we demonstrate that an invariant surface glycoprotein, ISG65, is a receptor for complement component 3 (C3). We show how ISG65 binds to the thioester domain of C3b. We also show that C3 contributes to control of trypanosomes during early infection in a mouse model and provide evidence that ISG65 is involved in reducing trypanosome susceptibility to C3-mediated clearance. Deposition of C3b on pathogen surfaces, such as trypanosomes, is a central point in activation of the complement"],"journal":["Nature communications"],"pubmed_title":["Invariant surface glycoprotein 65 of Trypanosoma brucei is a complement C3 receptor."],"pmcid":["PMC9424271"],"funding_grant_id":["217138/Z/19/Z","101020/Z/13/Z","MR/P001424/1"],"pubmed_authors":["Kimblin N","Pepperl J","Cook AD","Rust S","Webb H","Taylor MC","Francisco AF","Burns R","Voorheis P","Carrington M","Crow M","Trevor CE","Gibson W","Higgins MK","Schwede A","Macleod OJS","Peacock L","Seisenberger S","Redpath M"],"additional_accession":[]},"is_claimable":false,"name":"Invariant surface glycoprotein 65 of Trypanosoma brucei is a complement C3 receptor.","description":"African trypanosomes are extracellular pathogens of mammals and are exposed to the adaptive and innate immune systems. Trypanosomes evade the adaptive immune response through antigenic variation, but little is known about how they interact with components of the innate immune response, including complement. Here we demonstrate that an invariant surface glycoprotein, ISG65, is a receptor for complement component 3 (C3). We show how ISG65 binds to the thioester domain of C3b. We also show that C3 contributes to control of trypanosomes during early infection in a mouse model and provide evidence that ISG65 is involved in reducing trypanosome susceptibility to C3-mediated clearance. Deposition of C3b on pathogen surfaces, such as trypanosomes, is a central point in activation of the complement","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-31T16:02:37.053Z","creation":"2025-02-19T01:27:34.421Z"},"accession":"S-EPMC9424271","cross_references":{"pubmed":["36038546"],"doi":["10.1038/s41467-022-32728-9"]}}