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Human B-cell receptors (BCRs) specific for meningococcal capsular polysaccharide (MCPS) epitopes are membrane-bound immunoglobulins that mediate the recognition of Neisseria meningitidis (Pollard et al., 2009, Nature Reviews Immunology). These receptors are essential for the adaptive immune response, as they bind to the unique repeating carbohydrate structures of the bacterial capsule, which is the primary virulence factor and basis for serogroup classification (A, B, C, W, Y) (Stephens et al., 2007, The Lancet). Upon antigen binding, the BCR complex initiates intracellular signaling cascades that drive B-cell proliferation and differentiation into plasma cells that secrete protective antibodies capable of complement-mediated lysis (Janeway et al., 2001, Immunobiology). In the context of vaccination, these receptors are the primary targets for inducing protective immunity; conjugate vaccines are specifically designed to engage these BCRs while recruiting T-cell help to overcome the limitations of T-cell independent polysaccharide antigens (Borrow et al., 2013, Vaccine). A significant challenge in targeting these receptors involves Serogroup B, whose capsular polysaccharide mimics human neural cell adhesion molecules (NCAM-1), potentially leading to poor immunogenicity or theoretical risks of autoimmunity (Finne et al., 1983, The Lancet). Consequently, modern MenB vaccines often target surface proteins rather than the capsule to avoid these safety concerns while still providing protection (Pizza et al., 2020, Science Translational Medicine).
Meningococcal vaccine antigens bind to the B-cell receptor (BCR) on specific B-cell clones, inducing receptor clustering and intracellular signaling. In conjugate vaccines, the BCR-mediated internalization of the polysaccharide-protein complex allows for T-cell-dependent activation, leading to high-affinity IgG production and long-term memory (Borrow et al., 2013, Vaccine).
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