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The B-cell receptor (BCR) specific for Neisseria meningitidis capsular polysaccharide serogroup C is a membrane-bound immunoglobulin complex located on the surface of specific B lymphocytes [1]. Its primary biological function is the high-affinity recognition of the α(2→9)-linked sialic acid homopolymer that constitutes the MenC capsule [2]. Upon binding to its cognate antigen, the BCR triggers intracellular signaling pathways that lead to B-cell activation, proliferation, and differentiation into memory B cells and plasma cells [2]. This receptor is the fundamental target for meningococcal serogroup C conjugate vaccines, which are designed to overcome the T-cell independent nature of pure polysaccharides by linking them to carrier proteins [3]. The interaction between the vaccine antigen and the BCR is essential for inducing a robust, long-lasting immune response characterized by high titers of serum bactericidal antibodies (SBA) [1, 3]. These antibodies provide protection by facilitating complement-mediated lysis of the bacteria, thereby preventing invasive diseases such as meningitis and septicemia [4]. The BCR's ability to internalize the conjugated antigen for processing and presentation to T-helper cells is a key mechanism in the success of these vaccines [2]. Consequently, this receptor serves as the critical interface between the vaccine and the adaptive immune system to ensure long-term protection against Neisseria meningitidis [1]. Sources: [1] WHO (https://www.who.int/news-room/fact-sheets/detail/meningococcal-meningitis); [2] Pollard AJ, et al. Vaccine. 2000; [3] CDC (https://www.cdc.gov/vaccines/vpd/mening/hcp/index.html); [4] Borrow R, et al. Infect Immun. 2001.
Antigen binding to the B-cell receptor (BCR) triggers B-cell activation and, in the case of conjugate vaccines, receptor-mediated endocytosis for T-cell dependent immune responses, leading to the production of protective IgG antibodies and memory B cells [2, 3].
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