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Adaptive immune receptors recognizing Yersinia pestis F1 and V antigens comprise the specific B-cell receptors (BCRs) and T-cell receptors (TCRs) that identify the two most critical virulence factors of the plague-causing bacterium (Smiley, 2008, PMID: 18837787). The F1 (fraction 1) antigen forms a gelatinous capsule that prevents phagocytosis, while the V (LcrV) antigen is a key component of the Type III Secretion System (T3SS) tip complex, essential for injecting toxins into host cells (Hill et al., 1997, PMID: 9353040; Sun & Roland, 2014, PMID: 25566514). Recognition of these antigens by BCRs leads to the production of high-affinity IgG antibodies that neutralize the pathogen through opsonization and by blocking the T3SS-mediated suppression of the host immune system (Quenee et al., 2011, PMID: 21339304). TCRs recognize processed peptides of F1 and V presented on MHC molecules, triggering a Th1-polarized response characterized by IFN-gamma production, which is vital for activating cellular defense mechanisms (Smiley, 2008). These receptors are the primary targets of modern vaccine development, most notably the recombinant F1-V fusion protein (rF1-V), which is designed to elicit protective memory responses (Williamson & West, 2021, PMID: 34533433). Furthermore, monoclonal antibodies derived from these receptors are being investigated as potent post-exposure therapies to provide immediate, passive immunity against both bubonic and pneumonic plague (Quenee et al., 2011).
Vaccines induce the expansion of these receptors to provide memory; monoclonal antibodies act as exogenous receptors to neutralize F1 and V antigens, preventing bacterial capsule formation and Type III Secretion System function (Smiley, 2008; Quenee et al., 2011).
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