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The Streptococcus pneumoniae capsular polysaccharide serotype 18C (CPS 18C) is a major surface structure and key virulence factor produced by this gram-positive bacterium, which is a leading cause of pneumonia, meningitis, and otitis media. CPS 18C shields the bacterium from host immune clearance by inhibiting opsonophagocytosis, blocking complement activation, and impairing interactions with phagocytic receptors, thereby enabling nasal colonization, epithelial attachment, and invasive disease. Encoded by a specific cps locus between dexB and aliA genes, it features a polymerase-dependent assembly involving initial glucosyl-1-phosphate transfer by WchA, rhamnosyl transfer by WchF, and additional glycosyltransferases (WciU, WciV, WciW) plus glycerol-1-phosphate addition by WciY, forming a repeat unit with glucose, rhamnose, and glycerol branches translocated and polymerized for cell wall attachment. As a therapeutic target, CPS 18C is included in vaccines like PCV20, PCV21, and PPSV23, which elicit serotype-specific antibodies for opsonophagocytic killing, though challenges include limited cross-reactivity and post-vaccination shifts to non-vaccine serotypes. Its structure and biosynthesis genes show homology to other serotypes, aiding recombinant production studies for vaccine development.
Induction of serotype-specific opsonophagocytic antibodies that promote phagocytic clearance of encapsulated bacteria
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