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Article: Contribution of renal secreted complement C3 to the circulating pool in humans

TitleContribution of renal secreted complement C3 to the circulating pool in humans
Authors
Issue Date1999
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal Of Immunology, 1999, v. 162 n. 7, p. 4336-4341 How to Cite?
AbstractComplement C3 produced within the kidney may be an important mediator of local inflammatory and immunological injury. The overall level of renal C3 production and consequently its contribution to the total circulating C3 level are, however, unknown. This was investigated by using the conversion of C3 from recipient to donor allotype following renal transplantation. The C3 F and S allotypes of 80 consecutive renal donor-recipient pairs (148 individuals) were determined by amplification refractory mutation system analysis. The extent of allotype conversion in C3 F/S mismatched recipients was quantified at different stages after transplantation, using an enzyme- linked immunosorbent assay specific for the HAV 4-1 polymorphism of C3 that is strongly associated with C3F. Twenty-one of the eighty recipients were potentially informative, i.e., were C3 SS recipients of C3 FF or FS donor kidneys. In the early postoperative period, donor-derived C3 (HAV 4-1- positive) was undetectable, increasing to 9.6% of the total circulating C3 at times of acute allograft rejection. When graft dysfunction occurred from causes other than rejection, donor C3 remained undetectable. After stable graft function was attained (3-13 mo after transplantation), donor C3 made up 4.5% of the total circulating C3 pool. Our findings demonstrate that human transplant kidney in the resting state is a significant source of extrahepatic C3. Its heightened local synthesis during rejection episodes suggests a possible pathogenic role for C3 in this immunological process.
Persistent Identifierhttp://hdl.handle.net/10722/162352
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, Sen_US
dc.contributor.authorZhou, Wen_US
dc.contributor.authorSheerin, NSen_US
dc.contributor.authorVaughan, RWen_US
dc.contributor.authorSacks, SHen_US
dc.date.accessioned2012-09-05T05:19:12Z-
dc.date.available2012-09-05T05:19:12Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Immunology, 1999, v. 162 n. 7, p. 4336-4341en_US
dc.identifier.issn0022-1767en_US
dc.identifier.urihttp://hdl.handle.net/10722/162352-
dc.description.abstractComplement C3 produced within the kidney may be an important mediator of local inflammatory and immunological injury. The overall level of renal C3 production and consequently its contribution to the total circulating C3 level are, however, unknown. This was investigated by using the conversion of C3 from recipient to donor allotype following renal transplantation. The C3 F and S allotypes of 80 consecutive renal donor-recipient pairs (148 individuals) were determined by amplification refractory mutation system analysis. The extent of allotype conversion in C3 F/S mismatched recipients was quantified at different stages after transplantation, using an enzyme- linked immunosorbent assay specific for the HAV 4-1 polymorphism of C3 that is strongly associated with C3F. Twenty-one of the eighty recipients were potentially informative, i.e., were C3 SS recipients of C3 FF or FS donor kidneys. In the early postoperative period, donor-derived C3 (HAV 4-1- positive) was undetectable, increasing to 9.6% of the total circulating C3 at times of acute allograft rejection. When graft dysfunction occurred from causes other than rejection, donor C3 remained undetectable. After stable graft function was attained (3-13 mo after transplantation), donor C3 made up 4.5% of the total circulating C3 pool. Our findings demonstrate that human transplant kidney in the resting state is a significant source of extrahepatic C3. Its heightened local synthesis during rejection episodes suggests a possible pathogenic role for C3 in this immunological process.en_US
dc.languageengen_US
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_US
dc.relation.ispartofJournal of Immunologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAntibodies, Monoclonal - Blooden_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshChilden_US
dc.subject.meshComplement C3 - Immunology - Metabolism - Secretionen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Amplificationen_US
dc.subject.meshGraft Rejectionen_US
dc.subject.meshHumansen_US
dc.subject.meshKidney - Secretionen_US
dc.subject.meshKidney Diseasesen_US
dc.subject.meshKidney Transplantation - Immunologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPostoperative Perioden_US
dc.titleContribution of renal secreted complement C3 to the circulating pool in humansen_US
dc.typeArticleen_US
dc.identifier.emailTang, S:scwtang@hku.hken_US
dc.identifier.authorityTang, S=rp00480en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10201966-
dc.identifier.scopuseid_2-s2.0-0033120556en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033120556&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume162en_US
dc.identifier.issue7en_US
dc.identifier.spage4336en_US
dc.identifier.epage4341en_US
dc.identifier.isiWOS:000079278000080-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTang, S=7403437082en_US
dc.identifier.scopusauthoridZhou, W=7404515807en_US
dc.identifier.scopusauthoridSheerin, NS=6603806215en_US
dc.identifier.scopusauthoridVaughan, RW=7201482617en_US
dc.identifier.scopusauthoridSacks, SH=7103294121en_US

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