A functional and structural basis for TCR cross-resctivity in multiple sclerosis

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Standard

A functional and structural basis for TCR cross-resctivity in multiple sclerosis. / Lang, Heather L.E.; Jacobsen, Helle; Ikemizu, S.; Andersson, Christina; Harlos, Karl; Madsen, L.; Hjorth, Peter; Søndergaard, Leif; Svejgaard, Arne; Wucherpfennig, Kai; Stuart, David I.; Bell, John I.; Jones, Yvonne; Fugger, Lars.

I: Nature Immunology, Bind 3, Nr. 10, 2002, s. 940-943.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Lang, HLE, Jacobsen, H, Ikemizu, S, Andersson, C, Harlos, K, Madsen, L, Hjorth, P, Søndergaard, L, Svejgaard, A, Wucherpfennig, K, Stuart, DI, Bell, JI, Jones, Y & Fugger, L 2002, 'A functional and structural basis for TCR cross-resctivity in multiple sclerosis', Nature Immunology, bind 3, nr. 10, s. 940-943. https://doi.org/10.1038/ni835

APA

Lang, H. L. E., Jacobsen, H., Ikemizu, S., Andersson, C., Harlos, K., Madsen, L., Hjorth, P., Søndergaard, L., Svejgaard, A., Wucherpfennig, K., Stuart, D. I., Bell, J. I., Jones, Y., & Fugger, L. (2002). A functional and structural basis for TCR cross-resctivity in multiple sclerosis. Nature Immunology, 3(10), 940-943. https://doi.org/10.1038/ni835

Vancouver

Lang HLE, Jacobsen H, Ikemizu S, Andersson C, Harlos K, Madsen L o.a. A functional and structural basis for TCR cross-resctivity in multiple sclerosis. Nature Immunology. 2002;3(10):940-943. https://doi.org/10.1038/ni835

Author

Lang, Heather L.E. ; Jacobsen, Helle ; Ikemizu, S. ; Andersson, Christina ; Harlos, Karl ; Madsen, L. ; Hjorth, Peter ; Søndergaard, Leif ; Svejgaard, Arne ; Wucherpfennig, Kai ; Stuart, David I. ; Bell, John I. ; Jones, Yvonne ; Fugger, Lars. / A functional and structural basis for TCR cross-resctivity in multiple sclerosis. I: Nature Immunology. 2002 ; Bind 3, Nr. 10. s. 940-943.

Bibtex

@article{97d1098074c511dbbee902004c4f4f50,
title = "A functional and structural basis for TCR cross-resctivity in multiple sclerosis",
abstract = "The multiple sclerosis (MS)-associated HLA major histocompatibility complex (MHC) class II alleles DRB1*1501, DRB5*0101 and DQB1*0602 are in strong linkage disequilibrium, making it difficult to determine which is the principal MS risk gene. Here we show that together the DRB1 and DRB5 loci may influence susceptibility to MS. We demonstrate that a T cell receptor (TCR) from an MS patient recognized both a DRB1*1501-restricted myelin basic protein (MBP) and DRB5*0101-restricted Epstein-Barr virus (EBV) peptide. Crystal structure determination of the DRB5*0101-EBV peptide complex revealed a marked degree of structural equivalence to the DRB1*1501-MBP peptide complex at the surface presented for TCR recognition. This provides structural evidence for molecular mimicry involving HLA molecules. The structural details suggest an explanation for the preponderance of MHC class II associations in HLA-associated diseases.",
author = "Lang, {Heather L.E.} and Helle Jacobsen and S. Ikemizu and Christina Andersson and Karl Harlos and L. Madsen and Peter Hjorth and Leif S{\o}ndergaard and Arne Svejgaard and Kai Wucherpfennig and Stuart, {David I.} and Bell, {John I.} and Yvonne Jones and Lars Fugger",
year = "2002",
doi = "10.1038/ni835",
language = "English",
volume = "3",
pages = "940--943",
journal = "Nature Immunology",
issn = "1529-2908",
publisher = "nature publishing group",
number = "10",

}

RIS

TY - JOUR

T1 - A functional and structural basis for TCR cross-resctivity in multiple sclerosis

AU - Lang, Heather L.E.

AU - Jacobsen, Helle

AU - Ikemizu, S.

AU - Andersson, Christina

AU - Harlos, Karl

AU - Madsen, L.

AU - Hjorth, Peter

AU - Søndergaard, Leif

AU - Svejgaard, Arne

AU - Wucherpfennig, Kai

AU - Stuart, David I.

AU - Bell, John I.

AU - Jones, Yvonne

AU - Fugger, Lars

PY - 2002

Y1 - 2002

N2 - The multiple sclerosis (MS)-associated HLA major histocompatibility complex (MHC) class II alleles DRB1*1501, DRB5*0101 and DQB1*0602 are in strong linkage disequilibrium, making it difficult to determine which is the principal MS risk gene. Here we show that together the DRB1 and DRB5 loci may influence susceptibility to MS. We demonstrate that a T cell receptor (TCR) from an MS patient recognized both a DRB1*1501-restricted myelin basic protein (MBP) and DRB5*0101-restricted Epstein-Barr virus (EBV) peptide. Crystal structure determination of the DRB5*0101-EBV peptide complex revealed a marked degree of structural equivalence to the DRB1*1501-MBP peptide complex at the surface presented for TCR recognition. This provides structural evidence for molecular mimicry involving HLA molecules. The structural details suggest an explanation for the preponderance of MHC class II associations in HLA-associated diseases.

AB - The multiple sclerosis (MS)-associated HLA major histocompatibility complex (MHC) class II alleles DRB1*1501, DRB5*0101 and DQB1*0602 are in strong linkage disequilibrium, making it difficult to determine which is the principal MS risk gene. Here we show that together the DRB1 and DRB5 loci may influence susceptibility to MS. We demonstrate that a T cell receptor (TCR) from an MS patient recognized both a DRB1*1501-restricted myelin basic protein (MBP) and DRB5*0101-restricted Epstein-Barr virus (EBV) peptide. Crystal structure determination of the DRB5*0101-EBV peptide complex revealed a marked degree of structural equivalence to the DRB1*1501-MBP peptide complex at the surface presented for TCR recognition. This provides structural evidence for molecular mimicry involving HLA molecules. The structural details suggest an explanation for the preponderance of MHC class II associations in HLA-associated diseases.

U2 - 10.1038/ni835

DO - 10.1038/ni835

M3 - Journal article

VL - 3

SP - 940

EP - 943

JO - Nature Immunology

JF - Nature Immunology

SN - 1529-2908

IS - 10

ER -

ID: 134822