作者: Margaret K. Hostetter
DOI: 10.1128/9781555815820.CH7
关键词: Classical complement pathway 、 Microbiology 、 Factor H 、 Alternative complement pathway 、 Complement component 2 、 Complement system 、 Lectin pathway 、 Complement component 3 、 Complement factor B 、 Biology
摘要: This chapter briefly reviews some salient features of complement-mediated opsonophagocytosis. It discusses the inhibitory mechanisms attributed to specific pneumococcal proteins and polysaccharides, human immunodeficiencies particular relevance killing Streptococcus pneumoniae. Traditionally, binding complement protein C1q Fc portion either pentavalent immunoglobulin M (IgM) or IgG initiates classical pathway. The mannose-binding lectin (MBL) complex, composed three six subunits MBL, preferentially recognizes mannose, mannans, N-acetylglucosamine (GlcNAc). integrity alternative pathway is thought be critical for those hosts lacking type-specific anticapsular antibodies required activation (e.g., C2). Comparative studies bacteremia in C57BL/6 mice genetically deficient C1q, factor B (encoded by Bf), C3, C4, natural IgM pointed importance absence IgG. Exponentially growing wild-type S. pneumoniae strains serotypes 3, 4, 14 are able degrade both α- β-chains purified C3 other serum proteins. release pneumolysin (Ply) during autolysis leads pathway, possibly through At least proteins—pneumolysin, PhpA, Hic, PspC (CbpA/SpsA/PbcA), PspA, CppA—are now known interfere with opsonization phagocytic killing.