T-cell receptor recognizing Japanese encephalitis virus peptide-MHC complex (JEV-specific TCR)

T-cell receptors (TCRs) recognizing Japanese encephalitis virus (JEV) peptide–MHC complexes are the primary mediators of the adaptive cellular immune response against JEV infection. These receptors, expressed on the surface of CD8+ and CD4+ T cells, specifically bind to viral epitopes—most commonly derived from the NS3, NS5, and Envelope (E) proteins—that are presented by Major Histocompatibility Complex (MHC) molecules on the surface of infected cells or antigen-presenting cells (1.2.1, 1.4.4). Upon binding, the TCR initiates a signaling cascade that leads to T-cell activation, resulting in the production of pro-inflammatory cytokines like IFN-gamma and the direct lysis of JEV-infected cells by cytotoxic T lymphocytes (1.2.3, 1.4.3). In the context of therapeutic development, these TCRs are critical targets for vaccine design, where the goal is to elicit a robust and long-lasting population of JEV-specific memory T cells (1.3.3, 1.4.4). Furthermore, research into TCR-T cell therapy and CAR-T cells targeting pMHC complexes has identified these receptors as potential tools for treating severe viral infections or even certain cancers through oncolytic viral approaches (1.2.2, 1.3.5). Understanding the specificity and cross-reactivity of these TCRs is essential, as they can exhibit molecular mimicry with other flaviviruses such as Zika and Dengue, which may either provide cross-protection or contribute to immunopathology (1.3.4, 1.4.2).

Other names

Japanese encephalitis virus-specific T-cell receptorJEV-specific TCRJEV pMHC-specific TCRJEV-reactive T-cell receptor

Recognition of Japanese encephalitis virus (JEV)-derived peptides (typically from non-structural proteins like NS3 and NS5 or structural proteins like the E protein) presented by Major Histocompatibility Complex (MHC) class I or II molecules, which triggers T-cell activation, clonal expansion, and effector functions to eliminate infected cells.