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T-cell receptors (TCRs) are heterodimeric proteins expressed on the surface of T lymphocytes, usually composed of α and β chains, which specifically recognize peptides derived from pathogens (such as TBE virus) that are bound to major histocompatibility complex (MHC) molecules on antigen-presenting cells[1][3][5]. In the case of TBE virus infection or vaccination, viral peptides from the TBE virus are processed and presented by either MHC class I molecules (to CD8+ cytotoxic T cells) or MHC class II molecules (to CD4+ helper T cells)[4][6][8]. The TCR binds specifically to these peptide–MHC complexes, initiating T cell activation, which is critical for antiviral immune response and for the generation of immunological memory[1][3][5][6]. The structural specificity of the TCR-peptide-MHC interaction determines T cell specificity and helps distinguish between self and non-self antigens[1][7]. In the context of TBE virus, CD4+ and CD8+ T cell responses are important for immunity and can be characterized both after infection and vaccination[4][6]. No direct small-molecule drugs target this specific receptor–ligand pair clinically, but in principle, it constitutes a target for T cell-based immunotherapies or vaccine design.
Cellular immunity modulation (for TCR-targeting drugs or therapies, e.g., adoptive T cell therapy)
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