Potent T cell agonism mediated by a very rapid TCR/pMHC interaction.
The interaction between T cell receptors (TCR) and peptide-major histocompatibility complex (pMHC) antigens can lead to varying degrees of agonism (T cell activation), or antagonism. The P14 TCR recognises the lymphocytic choriomeningitis virus (LCMV)-derived peptide, gp33 residues 33-41 (KAVYNFATC)...
| Հիմնական հեղինակներ: | , , , , , |
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| Ձևաչափ: | Journal article |
| Լեզու: | English |
| Հրապարակվել է: |
2007
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| _version_ | 1826276129280884736 |
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| author | Boulter, J Schmitz, N Sewell, A Godkin, A Bachmann, M Gallimore, A |
| author_facet | Boulter, J Schmitz, N Sewell, A Godkin, A Bachmann, M Gallimore, A |
| author_sort | Boulter, J |
| collection | OXFORD |
| description | The interaction between T cell receptors (TCR) and peptide-major histocompatibility complex (pMHC) antigens can lead to varying degrees of agonism (T cell activation), or antagonism. The P14 TCR recognises the lymphocytic choriomeningitis virus (LCMV)-derived peptide, gp33 residues 33-41 (KAVYNFATC), presented in the context of H-2D(b). The cellular responses to various related H-2D(b) peptide ligands are very well characterised, and P14 TCR-transgenic mice have been used extensively in models of virus infection, autoimmunity and tumour rejection. Here, we analyse the binding of the P14 soluble TCR to a broad panel of related H-2D(b)-peptide complexes by surface plasmon resonance, and compare this with their diverse cellular responses. P14 TCR binds H-2D(b)-gp33 with a KD of 3 microM (+/-0.5 microM), typical of an immunodominant antiviral TCR, but with unusually fast kinetics (k(off) = 1 s(-1)), corresponding to a half-life of 0.7 s at 25 degrees C, outside the range previously observed for murine agonist TCR/pMHC interactions. The most striking feature of these data is that a very short half-life does not preclude the ability of a TCR/pMHC interaction to induce antiviral immunity, autoimmune disease and tumour rejection. |
| first_indexed | 2024-03-06T23:09:21Z |
| format | Journal article |
| id | oxford-uuid:64ee05f4-d1e6-4cee-8997-1edabb93c22b |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T23:09:21Z |
| publishDate | 2007 |
| record_format | dspace |
| spelling | oxford-uuid:64ee05f4-d1e6-4cee-8997-1edabb93c22b2022-03-26T18:22:10ZPotent T cell agonism mediated by a very rapid TCR/pMHC interaction.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:64ee05f4-d1e6-4cee-8997-1edabb93c22bEnglishSymplectic Elements at Oxford2007Boulter, JSchmitz, NSewell, AGodkin, ABachmann, MGallimore, AThe interaction between T cell receptors (TCR) and peptide-major histocompatibility complex (pMHC) antigens can lead to varying degrees of agonism (T cell activation), or antagonism. The P14 TCR recognises the lymphocytic choriomeningitis virus (LCMV)-derived peptide, gp33 residues 33-41 (KAVYNFATC), presented in the context of H-2D(b). The cellular responses to various related H-2D(b) peptide ligands are very well characterised, and P14 TCR-transgenic mice have been used extensively in models of virus infection, autoimmunity and tumour rejection. Here, we analyse the binding of the P14 soluble TCR to a broad panel of related H-2D(b)-peptide complexes by surface plasmon resonance, and compare this with their diverse cellular responses. P14 TCR binds H-2D(b)-gp33 with a KD of 3 microM (+/-0.5 microM), typical of an immunodominant antiviral TCR, but with unusually fast kinetics (k(off) = 1 s(-1)), corresponding to a half-life of 0.7 s at 25 degrees C, outside the range previously observed for murine agonist TCR/pMHC interactions. The most striking feature of these data is that a very short half-life does not preclude the ability of a TCR/pMHC interaction to induce antiviral immunity, autoimmune disease and tumour rejection. |
| spellingShingle | Boulter, J Schmitz, N Sewell, A Godkin, A Bachmann, M Gallimore, A Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. |
| title | Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. |
| title_full | Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. |
| title_fullStr | Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. |
| title_full_unstemmed | Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. |
| title_short | Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. |
| title_sort | potent t cell agonism mediated by a very rapid tcr pmhc interaction |
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