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The human adaptive and innate immune receptors recognizing Salmonella typhi antigens represent a diverse group of host proteins that detect and respond to the causative agent of typhoid fever. Innate recognition is mediated by pattern recognition receptors (PRRs) such as Toll-like receptor 4 (TLR4), which recognizes lipopolysaccharide (LPS), and Toll-like receptor 5 (TLR5), which detects flagellin (FliC) (2.3.3, 2.4.2). Intracellular sensors like the NLRC4 inflammasome also play a critical role by recognizing flagellin and type III secretion system components in the cytosol (2.4.2, 2.4.5). Furthermore, the C-type lectin receptor DC-SIGN (CD209) and membrane prohibitin have been identified as specific receptors for the Vi capsular polysaccharide, a key virulence factor of S. typhi (2.2.1, 2.2.5). The adaptive immune response is orchestrated by T-cell receptors (TCRs) and B-cell receptors (BCRs) that recognize specific bacterial antigens to generate long-term protective immunity (2.3.1, 2.3.2). These receptors are the primary targets of typhoid vaccines, including the Vi capsular polysaccharide vaccine and the live-attenuated Ty21a strain, which aim to elicit high-titer antibodies and memory T-cell responses (2.2.3, 2.2.4). However, S. typhi employs various evasion strategies, such as downregulating flagellin and using the Vi capsule to mask surface antigens, to avoid detection by these receptors (2.1.2, 2.2.4).
Vaccines stimulate these receptors to induce innate signaling and adaptive immune memory against Salmonella typhi antigens, leading to the production of protective antibodies and the activation of Th1 and Th17 cellular immunity.
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