Prevention of C3 deposition by capsular polysaccharide is a virulence mechanism of type III group B streptococci.
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A critical role of natural immunoglobulin M in immediate defense against systemic bacterial infectionUnderstanding the regulation of Group B Streptococcal virulence factorsRecent advances in understanding the molecular basis of group B Streptococcus virulenceInnate immune response to Streptococcus iniae infection in zebrafish larvae.Discovery and characterization of sialic acid O-acetylation in group B Streptococcus.Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid.Capsular polysaccharide regulates neutrophil complement receptor interactions with type III group B streptococciRestricted ability of group B streptococcal C5a-ase to inactivate C5a prepared from different animal species.Correlation between Group B Streptococcal Genotypes, Their Antimicrobial Resistance Profiles, and Virulence Genes among Pregnant Women in Lebanon.Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.Ubiquitous sialometabolism present among oral fusobacteriaSurface proteins of Streptococcus agalactiae and related proteins in other bacterial pathogens.Structural and genetic diversity of group B streptococcus capsular polysaccharides.Genome sequence of Streptococcus gallolyticus: insights into its adaptation to the bovine rumen and its ability to cause endocarditis.Evaluation of the Immunomodulatory Properties of Streptococcus suis and Group B Streptococcus Capsular Polysaccharides on the Humoral Response.Anchors away: contribution of a glycolipid anchor to bacterial invasion of host cells.Regulation of cell component production by growth rate in the group B Streptococcus.Capsular sialic acid limits C5a production on type III group B streptococci.Role of macrophage sialoadhesin in host defense against the sialylated pathogen group B Streptococcus.The interplay between Siglecs and sialylated pathogensImmunomodulatory effects of Streptococcus suis capsule type on human dendritic cell responses, phagocytosis and intracellular survival.Multifarious roles of sialic acids in immunity.Membrane topology and DNA-binding ability of the Streptococcal CpsA proteinInduction of tumor necrosis factor alpha by the group- and type-specific polysaccharides from type III group B streptococci.The Vi capsular polysaccharide prevents complement receptor 3-mediated clearance of Salmonella enterica serotype Typhi.Group B streptococcus-induced nitric oxide production in murine macrophages is CR3 (CD11b/CD18) dependent.Of mice and men, revisited: new insights into an ancient molecule from studies of complement activation by Cryptococcus neoformansThe Streptococcus pneumoniae capsule inhibits complement activity and neutrophil phagocytosis by multiple mechanismsCommensal Streptococcus agalactiae isolated from patients seen at University Hospital of Londrina, Paraná, Brazil: capsular types, genotyping, antimicrobial susceptibility and virulence determinantsGroup B Streptococcus engages an inhibitory Siglec through sialic acid mimicry to blunt innate immune and inflammatory responses in vivoThe sensor histidine kinase RgfC affects group B streptococcal virulence factor expression independent of its response regulator RgfA.The Delta subunit of RNA polymerase is required for virulence of Streptococcus agalactiae.Procession to pediatric bacteremia and sepsis: covert operations and failures in diplomacyImmune activation and suppression by group B streptococcus in a murine model of urinary tract infectionPenicillin-binding protein 1a promotes resistance of group B streptococcus to antimicrobial peptides.Impaired phagocytosis and opsonisation towards group B streptococci in preterm neonatesStreptococcus agalactiae capsule polymer length and attachment is determined by the proteins CpsABCD.Role of C5a-ase in group B streptococcal resistance to opsonophagocytic killing.Cell growth rate regulates expression of group B Streptococcus type III capsular polysaccharide.Interleukin-12 and tumor necrosis factor alpha mediate innate production of gamma interferon by group B Streptococcus-treated splenocytes of severe combined immunodeficiency mice.
P2860
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P2860
Prevention of C3 deposition by capsular polysaccharide is a virulence mechanism of type III group B streptococci.
description
1992 nî lūn-bûn
@nan
1992年の論文
@ja
1992年論文
@yue
1992年論文
@zh-hant
1992年論文
@zh-hk
1992年論文
@zh-mo
1992年論文
@zh-tw
1992年论文
@wuu
1992年论文
@zh
1992年论文
@zh-cn
name
Prevention of C3 deposition by ...... type III group B streptococci.
@en
type
label
Prevention of C3 deposition by ...... type III group B streptococci.
@en
prefLabel
Prevention of C3 deposition by ...... type III group B streptococci.
@en
P2093
P2860
P1476
Prevention of C3 deposition by ...... type III group B streptococci.
@en
P2093
D L Kasper
M B Marques
M K Pangburn
M R Wessels
P2860
P304
P407
P577
1992-10-01T00:00:00Z