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Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction

The structural requirements for signal transduction by class I major histocompatibility complex (MHC) molecules were examined. Native or mutant HLA-A2 or HLA-B27 constructs lacking most of their cytoplasmic domains were co-transfected with pSV2neo into Jurkat cells. Transfection of either native or...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1990
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2188606/
https://www.ncbi.nlm.nih.gov/pubmed/2212953
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description The structural requirements for signal transduction by class I major histocompatibility complex (MHC) molecules were examined. Native or mutant HLA-A2 or HLA-B27 constructs lacking most of their cytoplasmic domains were co-transfected with pSV2neo into Jurkat cells. Transfection of either native or mutant constructs resulted in a comparable expression of the gene products. Stimulation of transfectants expressing either native or truncated A2 or B27 molecules with specific mAb evoked an increase in [Ca2+]i upon crosslinking. Moreover, crosslinking native or truncated A2 or B27 induced IL-2 production upon co-stimulation with phorbol myristate acetate. These results confirm that crosslinking class I MHC molecules transduces an activation signal to human T cells. Effective signaling was observed when all but four of the intracytoplasmic residues were deleted, indicating that signal transduction does not require this portion of the molecule.
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spelling pubmed-21886062008-04-17 Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction J Exp Med Articles The structural requirements for signal transduction by class I major histocompatibility complex (MHC) molecules were examined. Native or mutant HLA-A2 or HLA-B27 constructs lacking most of their cytoplasmic domains were co-transfected with pSV2neo into Jurkat cells. Transfection of either native or mutant constructs resulted in a comparable expression of the gene products. Stimulation of transfectants expressing either native or truncated A2 or B27 molecules with specific mAb evoked an increase in [Ca2+]i upon crosslinking. Moreover, crosslinking native or truncated A2 or B27 induced IL-2 production upon co-stimulation with phorbol myristate acetate. These results confirm that crosslinking class I MHC molecules transduces an activation signal to human T cells. Effective signaling was observed when all but four of the intracytoplasmic residues were deleted, indicating that signal transduction does not require this portion of the molecule. The Rockefeller University Press 1990-10-01 /pmc/articles/PMC2188606/ /pubmed/2212953 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
Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction
title Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction
title_full Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction
title_fullStr Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction
title_full_unstemmed Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction
title_short Analysis of T cell signaling by class I MHC molecules: the cytoplasmic domain is not required for signal transduction
title_sort analysis of t cell signaling by class i mhc molecules: the cytoplasmic domain is not required for signal transduction
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2188606/
https://www.ncbi.nlm.nih.gov/pubmed/2212953