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A Dominant Complement Fixation Pathway for Pneumococcal Polysaccharides Initiated by SIGN-R1 Interacting with C1q

DC FieldValueLanguage
dc.contributor.author박채규-
dc.date.accessioned2015-06-10T13:09:38Z-
dc.date.available2015-06-10T13:09:38Z-
dc.date.issued2006-
dc.identifier.issn0092-8674-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/111120-
dc.description.abstractThe intricate system of serum complement proteins provides resistance to infection. A pivotal step in the complement pathway is the assembly of a C3 convertase, which digests the C3 complement component to form microbial binding C3 fragments recognized by leukocytes. The spleen and C3 provide resistance against blood-borne S. pneumoniae infection. To better understand the mechanisms involved, we studied SIGN-R1, a lectin that captures microbial polysaccharides in spleen. Surprisingly, conditional SIGN-R1 knockout mice developed deficits in C3 catabolism when given S. pneumoniae or its capsular polysaccharide intravenously. There were marked reductions in proteolysis of serum C3, deposition of C3 on organisms within SIGN-R1+ spleen macrophages, and formation of C3 ligands. We found that SIGN-R1 directly bound the complement C1 subcomponent, C1q, and assembled a C3 convertase, but without the traditional requirement for either antibody or factor B. The transmembrane lectin SIGN-R1 therefore contributes to innate resistance by an unusual C3 activation pathway.-
dc.description.statementOfResponsibilityopen-
dc.format.extent47~58-
dc.relation.isPartOfCELL-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAntigen-Antibody Reactions/immunology-
dc.subject.MESHCHO Cells-
dc.subject.MESHCell Adhesion Molecules/metabolism*-
dc.subject.MESHComplement Activation/immunology*-
dc.subject.MESHComplement C1q/immunology*-
dc.subject.MESHComplement C1q/metabolism*-
dc.subject.MESHComplement C3/chemistry-
dc.subject.MESHComplement C3/metabolism-
dc.subject.MESHComplement Pathway, Classical/immunology-
dc.subject.MESHCricetinae-
dc.subject.MESHCricetulus-
dc.subject.MESHFibroblasts/cytology-
dc.subject.MESHHumans-
dc.subject.MESHLectins, C-Type/metabolism*-
dc.subject.MESHMacrophages/cytology-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred BALB C-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMice, Knockout-
dc.subject.MESHPolysaccharides, Bacterial/immunology*-
dc.subject.MESHProtein Binding-
dc.subject.MESHReceptors, Cell Surface/metabolism*-
dc.subject.MESHSpleen/cytology-
dc.subject.MESHStreptococcus pneumoniae/immunology*-
dc.titleA Dominant Complement Fixation Pathway for Pneumococcal Polysaccharides Initiated by SIGN-R1 Interacting with C1q-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorYoung-Sun Kang-
dc.contributor.googleauthorYoonkyung Do-
dc.contributor.googleauthorHae-Kyung Lee-
dc.contributor.googleauthorSung Ho Park-
dc.contributor.googleauthorCheolho Cheong-
dc.contributor.googleauthorRebecca M. Lynch-
dc.contributor.googleauthorJutta M. Loeffler-
dc.contributor.googleauthorRalph M. Steinman-
dc.contributor.googleauthorChae Gyu Park-
dc.identifier.doi10.1016/j.cell.2006.01.046-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01718-
dc.relation.journalcodeJ00472-
dc.identifier.eissn1097-4172-
dc.identifier.pmid16615889-
dc.contributor.alternativeNamePark, Chae Gyu-
dc.contributor.affiliatedAuthorPark, Chae Gyu-
dc.rights.accessRightsfree-
dc.citation.volume125-
dc.citation.number1-
dc.citation.startPage47-
dc.citation.endPage58-
dc.identifier.bibliographicCitationCELL, Vol.125(1) : 47-58, 2006-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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