CD4+ T-cell receptor recognizing Varicella-Zoster Virus glycoprotein E-derived peptide–MHC class II complex (VZV gE-specific CD4+ TCR)

CD4+ T-cell receptors (TCRs) that specifically recognize peptides derived from the Varicella-Zoster Virus (VZV) glycoprotein E (gE) presented on MHC class II molecules are critical components of the adaptive immune system's defense against viral reactivation. Glycoprotein E is the most prevalent and immunogenic surface protein of VZV, serving as a key target for both natural and vaccine-induced immunity (Cunningham et al., 2016, NEJM). Upon recognition of the gE-peptide-MHC II complex, these TCRs initiate signaling cascades that lead to the activation and proliferation of CD4+ T helper cells, which secrete essential cytokines such as IFN-gamma and IL-2 to control viral replication (Bharucha et al., 2021, Frontiers in Immunology). This specific T-cell population is vital for preventing herpes zoster (shingles) and its complications, such as post-herpetic neuralgia, particularly in aging populations where T-cell immunity naturally declines (Levin et al., 2008, JID). Therapeutic strategies, most notably the recombinant zoster vaccine (Shingrix), utilize purified gE protein combined with the AS01B adjuvant system to specifically stimulate and maintain high frequencies of these gE-specific CD4+ T cells (Didierlaurent et al., 2014, Journal of Immunology).

Other names

Varicella-Zoster Virus glycoprotein E-specific T-cell receptorgE-specific CD4+ TCRVZV gE-MHC II-specific TCRGlycoprotein E-specific CD4+ T-cell receptor

Vaccines deliver glycoprotein E (gE) antigens which are processed by antigen-presenting cells and presented via MHC class II molecules to activate and expand gE-specific CD4+ T cells, providing protective immunity against VZV reactivation.