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T cell receptors (TCRs) recognizing rabies virus glycoprotein (G)-derived peptides are critical components of the adaptive immune system's defense against rabies virus infection. These receptors, located on the surface of T lymphocytes, specifically bind to viral peptides presented by Human Leukocyte Antigen (HLA) class I (for CD8+ cytotoxic T cells) and class II (for CD4+ helper T cells) molecules (Celis et al., 1988, J. Immunol.). The glycoprotein is the major surface antigen of the rabies virus and the primary target for both neutralizing antibodies and cellular immune responses (Xiang et al., 1995, Virology). Activation of these TCRs leads to the production of cytokines, the killing of infected cells, and the provision of help to B cells for antibody production (Lafage et al., 1990, J. Gen. Virol.). Understanding the specificity and repertoire of these TCRs is essential for the development of more effective rabies vaccines and potential immunotherapies, particularly in post-exposure prophylaxis scenarios where rapid and robust immune activation is required to prevent the virus from reaching the central nervous system (Ertl et al., 1989, Rev. Infect. Dis.).
Recognition of rabies virus glycoprotein-derived peptides presented by Human Leukocyte Antigen (HLA) class I or II molecules, triggering T cell activation, proliferation, and the orchestration of an adaptive immune response against the rabies virus.
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