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Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells

It has been established that at least some V beta 17+ T cells interact with an endogenous superantigen encoded by the murine retrovirus, Mtv- 9. To analyze the role of major histocompatibility complex (MHC) class II molecules in presenting the Mtv-9 encoded superantigen, vSAG-9 to V beta 17+ hybrido...

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Detalles Bibliográficos
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119304/
https://www.ncbi.nlm.nih.gov/pubmed/1535369
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description It has been established that at least some V beta 17+ T cells interact with an endogenous superantigen encoded by the murine retrovirus, Mtv- 9. To analyze the role of major histocompatibility complex (MHC) class II molecules in presenting the Mtv-9 encoded superantigen, vSAG-9 to V beta 17+ hybridomas, a panel of nine hybridomas was tested for their ability to respond to A20/2J (H-2d) and LBK (H-2a) cells which had been transfected with the vSAG-9 gene. Whereas some of the hybridomas recognized vSAG-9 exclusively in the context of H-2a, other hybridomas recognized vSAG-9 exclusively in the context of H-2d or in the context of both H-2d and H-2a. These results suggest that: (a) the class II MHC molecule plays a direct role in the recognition of retroviral superantigen by T cells, rather than serving simply as a platform for presentation; and, (b) it is likely that components of the TCR other than V beta are involved in the vSAG-9/TCR/class II interaction.
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spelling pubmed-21193042008-04-16 Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells J Exp Med Articles It has been established that at least some V beta 17+ T cells interact with an endogenous superantigen encoded by the murine retrovirus, Mtv- 9. To analyze the role of major histocompatibility complex (MHC) class II molecules in presenting the Mtv-9 encoded superantigen, vSAG-9 to V beta 17+ hybridomas, a panel of nine hybridomas was tested for their ability to respond to A20/2J (H-2d) and LBK (H-2a) cells which had been transfected with the vSAG-9 gene. Whereas some of the hybridomas recognized vSAG-9 exclusively in the context of H-2a, other hybridomas recognized vSAG-9 exclusively in the context of H-2d or in the context of both H-2d and H-2a. These results suggest that: (a) the class II MHC molecule plays a direct role in the recognition of retroviral superantigen by T cells, rather than serving simply as a platform for presentation; and, (b) it is likely that components of the TCR other than V beta are involved in the vSAG-9/TCR/class II interaction. The Rockefeller University Press 1992-07-01 /pmc/articles/PMC2119304/ /pubmed/1535369 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells
title Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells
title_full Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells
title_fullStr Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells
title_full_unstemmed Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells
title_short Major histocompatibility complex-restricted recognition of retroviral superantigens by V beta 17+ T cells
title_sort major histocompatibility complex-restricted recognition of retroviral superantigens by v beta 17+ t cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119304/
https://www.ncbi.nlm.nih.gov/pubmed/1535369