1ymm

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(New page: 200px<br /> <applet load="1ymm" size="450" color="white" frame="true" align="right" spinBox="true" caption="1ymm, resolution 3.500&Aring;" /> '''TCR/HLA-DR2b/MBP-p...)
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[[Image:1ymm.gif|left|200px]]<br />
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[[Image:1ymm.gif|left|200px]]<br /><applet load="1ymm" size="350" color="white" frame="true" align="right" spinBox="true"
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<applet load="1ymm" size="450" color="white" frame="true" align="right" spinBox="true"
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caption="1ymm, resolution 3.500&Aring;" />
caption="1ymm, resolution 3.500&Aring;" />
'''TCR/HLA-DR2b/MBP-peptide complex'''<br />
'''TCR/HLA-DR2b/MBP-peptide complex'''<br />
==Overview==
==Overview==
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Autoimmune diseases are caused by self-reactive lymphocytes that have, escaped deletion. Here we have determined the structure of the, trimolecular complex for a T cell receptor (TCR) from a patient with, multiple sclerosis that causes autoimmunity in transgenic mice. The, structure showed a TCR topology notably different from that of, antimicrobial TCRs. Rather than being centered on the peptide-major, histocompatibility complex, this TCR contacted only the N-terminal peptide, segment and made asymmetrical interactions with the major, histocompatibility complex helices. The interaction was dominated by the, hypervariable complementarity-determining region 3 loops, indicating that, unconventional topologies are possible because of the unique, complementarity-determining region 3 sequences created during, rearrangement. This topology reduces the interaction surface with peptide, and alters the geometry for CD4 association. We propose that unusual, TCR-binding properties can permit autoreactive T cells to escape deletion.
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Autoimmune diseases are caused by self-reactive lymphocytes that have escaped deletion. Here we have determined the structure of the trimolecular complex for a T cell receptor (TCR) from a patient with multiple sclerosis that causes autoimmunity in transgenic mice. The structure showed a TCR topology notably different from that of antimicrobial TCRs. Rather than being centered on the peptide-major histocompatibility complex, this TCR contacted only the N-terminal peptide segment and made asymmetrical interactions with the major histocompatibility complex helices. The interaction was dominated by the hypervariable complementarity-determining region 3 loops, indicating that unconventional topologies are possible because of the unique complementarity-determining region 3 sequences created during rearrangement. This topology reduces the interaction surface with peptide and alters the geometry for CD4 association. We propose that unusual TCR-binding properties can permit autoreactive T cells to escape deletion.
==Disease==
==Disease==
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==About this Structure==
==About this Structure==
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1YMM is a [http://en.wikipedia.org/wiki/Protein_complex Protein complex] structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] with NAG as [http://en.wikipedia.org/wiki/ligand ligand]. Full crystallographic information is available from [http://ispc.weizmann.ac.il/oca-bin/ocashort?id=1YMM OCA].
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1YMM is a [http://en.wikipedia.org/wiki/Protein_complex Protein complex] structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] with <scene name='pdbligand=NAG:'>NAG</scene> as [http://en.wikipedia.org/wiki/ligand ligand]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1YMM OCA].
==Reference==
==Reference==
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[[Category: Protein complex]]
[[Category: Protein complex]]
[[Category: Hahn, M.]]
[[Category: Hahn, M.]]
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[[Category: Nicholson, M.J.]]
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[[Category: Nicholson, M J.]]
[[Category: Pyrdol, J.]]
[[Category: Pyrdol, J.]]
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[[Category: Wucherpfennig, K.W.]]
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[[Category: Wucherpfennig, K W.]]
[[Category: NAG]]
[[Category: NAG]]
[[Category: auto-immunity]]
[[Category: auto-immunity]]
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[[Category: t cell repertoire]]
[[Category: t cell repertoire]]
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''Page seeded by [http://ispc.weizmann.ac.il/oca OCA ] on Mon Nov 12 20:21:49 2007''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 16:06:53 2008''

Revision as of 14:06, 21 February 2008


1ymm, resolution 3.500Å

Drag the structure with the mouse to rotate

TCR/HLA-DR2b/MBP-peptide complex

Contents

Overview

Autoimmune diseases are caused by self-reactive lymphocytes that have escaped deletion. Here we have determined the structure of the trimolecular complex for a T cell receptor (TCR) from a patient with multiple sclerosis that causes autoimmunity in transgenic mice. The structure showed a TCR topology notably different from that of antimicrobial TCRs. Rather than being centered on the peptide-major histocompatibility complex, this TCR contacted only the N-terminal peptide segment and made asymmetrical interactions with the major histocompatibility complex helices. The interaction was dominated by the hypervariable complementarity-determining region 3 loops, indicating that unconventional topologies are possible because of the unique complementarity-determining region 3 sequences created during rearrangement. This topology reduces the interaction surface with peptide and alters the geometry for CD4 association. We propose that unusual TCR-binding properties can permit autoreactive T cells to escape deletion.

Disease

Known diseases associated with this structure: Chronic infections, due to MBL deficiency OMIM:[154545], Diabetes mellitus, gestational, susceptibility to OMIM:[154545], Mannose-binding protein deficiency OMIM:[154545], Meningococcal disease, susceptibility to OMIM:[154545]

About this Structure

1YMM is a Protein complex structure of sequences from Homo sapiens with as ligand. Full crystallographic information is available from OCA.

Reference

Unconventional topology of self peptide-major histocompatibility complex binding by a human autoimmune T cell receptor., Hahn M, Nicholson MJ, Pyrdol J, Wucherpfennig KW, Nat Immunol. 2005 May;6(5):490-6. Epub 2005 Apr 10. PMID:15821740

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