{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["3"],"submitter":["Caesar JJ"],"funding":["Action Medical Research","Oxford Martin School, University of Oxford","Medical Research Council","Imperial College London","European Commission","Wellcome Trust"],"pubmed_abstract":["Genome-wide association studies have found variation within the complement factor H gene family links to host susceptibility to meningococcal disease caused by infection with Neisseria meningitidis (Davila et al., 2010). Mechanistic insights have been challenging since variation within this locus is complex and biological roles of the factor H-related proteins, unlike factor H, are incompletely understood. N. meningitidis subverts immune responses by hijacking a host-immune regulator, complement factor H (CFH), to the bacterial surface (Schneider et al., 2006; Madico et al., 2007; Schneider et al., 2009). We demonstrate that complement factor-H related 3 (CFHR3) promotes immune activation by acting as an antagonist of CFH. Conserved sequences between CFH and CFHR3 mean that the bacterium c"],"journal":["eLife"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4273445"],"repository":["biostudies-literature"],"pubmed_title":["Competition between antagonistic complement factors for a single protein on N. meningitidis rules disease susceptibility."],"pmcid":["PMC4273445"],"funding_grant_id":["098476","WT102908MA","102908/Z/13/Z","100298/Z/12/Z","2205","082291","G0900888","Vaccine Design","102908","100298","EUCLIDS FP7 GA no. 279185","Research Fellowship","WT082291MA"],"pubmed_authors":["Exley RM","Malik TH","Chittock E","Ward PN","Goiecoechea De Jorge E","Tang CM","Caesar JJ","Eaton J","Pickering MC","Lavender H","Lea SM"],"additional_accession":[]},"is_claimable":false,"name":"Competition between antagonistic complement factors for a single protein on N. meningitidis rules disease susceptibility.","description":"Genome-wide association studies have found variation within the complement factor H gene family links to host susceptibility to meningococcal disease caused by infection with Neisseria meningitidis (Davila et al., 2010). Mechanistic insights have been challenging since variation within this locus is complex and biological roles of the factor H-related proteins, unlike factor H, are incompletely understood. N. meningitidis subverts immune responses by hijacking a host-immune regulator, complement factor H (CFH), to the bacterial surface (Schneider et al., 2006; Madico et al., 2007; Schneider et al., 2009). We demonstrate that complement factor-H related 3 (CFHR3) promotes immune activation by acting as an antagonist of CFH. Conserved sequences between CFH and CFHR3 mean that the bacterium c","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Dec","modification":"2026-04-07T14:44:37.236Z","creation":"2019-03-27T01:42:11Z"},"accession":"S-EPMC4273445","cross_references":{"pubmed":["25534642"],"doi":["10.7554/eLife.04008"]}}