| Variable influence of MHC polymorphism on the recognition of bacterial superantigens by T cells. | |
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MedLine Citation:
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PMID: 7636239 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Superantigen recognition by some T cells is strongly influenced by polymorphic residues of the MHC class II molecule, suggesting that the TCR contacts the class II molecule during superantigen engagement. However, the degree of MHC preference varies with V beta expression. For example, the recognition of staphylococcal enterotoxin B (SEB) by murine V beta 14+ T cell hybridomas is strongly influenced by MHC polymorphism, whereas the recognition of SEB by V beta 8.2+ hybridomas appears to be independent of MHC polymorphism. One possible explanation for this difference is that V beta 14+ TCR may have a lower avidity for SEB such that the stability of the TCR/SEB/MHC complex is more strongly influenced by potential TCR/MHC interactions. To investigate this possibility, we examined the MHC preference of SEB recognition by murine V beta 8.2+/CD4+ T cell hybridomas in which we altered the strength of SEB recognition. First, we compared the recognition of wild-type SEB and mutant SEB, which only weakly activates T cells. Second, we compared recognition of SEB presented by I-E and I-A molecules, which differ in their affinity for SEB. In both cases, the degree of MHC preference was significantly increased when the strength of SEB recognition was reduced. Furthermore, we used mutant MHC class II molecules to show that the degree of MHC preference was controlled by residues of the class II molecule predicted to interact with the TCR during SEB recognition. Taken together, these data support the idea that there is a TCR/MHC interaction during SEB recognition, and the influence of this interaction varies with the overall avidity of the TCR/SEB/MHC complex. |
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Authors:
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R Wen; M A Blackman; D L Woodland |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 155 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 1995 Aug |
Date Detail:
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Created Date: 1995-09-08 Completed Date: 1995-09-08 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1884-92 Citation Subset: AIM; IM |
Affiliation:
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Department of Pathology, University of Tennessee, Memphis 38163, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Line Enterotoxins / immunology* Histocompatibility Antigens Class II / immunology Hybridomas / immunology Major Histocompatibility Complex* Mice Mice, Inbred C57BL Polymorphism, Genetic Receptors, Antigen, T-Cell, alpha-beta / analysis, physiology* Staphylococcus aureus / immunology* Superantigens / immunology* T-Lymphocytes / immunology* |
| Grant Support | |
ID/Acronym/Agency:
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AI-31489/AI/NIAID NIH HHS; CA-56570/CA/NCI NIH HHS; P30 CA-21765/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enterotoxins; 0/Histocompatibility Antigens Class II; 0/Receptors, Antigen, T-Cell, alpha-beta; 0/Superantigens; 39424-53-8/enterotoxin B, staphylococcal |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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