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The T-cell receptor (TCR) recognizing Varicella-Zoster Virus (VZV) glycoprotein E (gE) peptides on MHC class II is a critical component of the cellular immune response against shingles. Glycoprotein E is the most prevalent surface protein of VZV and serves as the primary antigen for both humoral and cell-mediated immunity (UniProt P09333). These specific TCRs are expressed on CD4+ T cells, which identify gE fragments presented by Major Histocompatibility Complex (MHC) class II molecules on the surface of antigen-presenting cells (PMID: 30104354). Activation of these TCRs leads to the expansion of memory T cells and the production of effector cytokines like interferon-gamma, which are vital for suppressing VZV reactivation from sensory ganglia (PMID: 29653957). This target is the central focus of the recombinant zoster vaccine (Shingrix), which utilizes a truncated form of gE and an adjuvant system to boost the frequency and polyfunctionality of these specific T cells. Understanding the repertoire and binding affinity of these TCRs is essential for evaluating vaccine efficacy and developing next-generation immunotherapies for VZV-related complications.
Binding of the T-cell receptor to the glycoprotein E peptide-MHC class II complex triggers CD4+ T-cell activation and Th1 cytokine release, providing cellular immunity against Varicella-Zoster Virus.
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