T-cell receptor recognizing dengue virus envelope protein-derived peptides (TCR-DENV-E)

T-cell receptors (TCRs) recognizing dengue virus (DENV) envelope (E) protein-derived peptides presented by the Major Histocompatibility Complex (MHC) are essential mediators of the adaptive immune response to dengue infection. These TCRs are expressed on the surface of CD8+ and CD4+ T cells and function by binding to specific viral epitopes displayed by MHC Class I or Class II molecules, respectively [1][2]. This interaction is the primary step in T-cell activation, leading to the elimination of virus-infected cells and the orchestration of a broader immune response through cytokine secretion [3]. In the context of dengue, the specificity of these TCRs is critical because the virus exists as four distinct serotypes; sub-optimal or cross-reactive TCR binding can lead to "original antigenic sin," a phenomenon where a suboptimal immune response contributes to severe disease manifestations such as Dengue Hemorrhagic Fever [4]. Consequently, these TCRs are primary targets for vaccine design and are being explored for use in TCR-engineered T-cell therapies to provide robust, cross-protective immunity [1]. Monitoring the frequency and phenotype of T cells bearing these receptors serves as a vital biomarker for assessing vaccine efficacy and disease progression [3].

Other names

DENV-specific TCRDengue virus envelope-specific T-cell receptorMHC-restricted DENV-E TCRDengue E-peptide-MHC-TCR complex

The T-cell receptor (TCR) recognizes specific peptides derived from the dengue virus envelope protein when presented by MHC molecules. This binding event triggers the TCR-CD3 complex signaling pathway, leading to T-cell activation, proliferation, and the execution of effector functions such as the release of cytotoxic granules and pro-inflammatory cytokines to eliminate infected cells.