Imperial College London

DrRichardNicholas

Faculty of MedicineDepartment of Brain Sciences

Professor of Practice (Neurology)
 
 
 
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Contact

 

r.nicholas

 
 
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Location

 

12L12CLab BlockCharing Cross Campus

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Summary

 

Publications

Citation

BibTex format

@article{Durrenberger:2012:10.1111/imm.12012.,
author = {Durrenberger, PF and Webb, LV and Sim, MJ and Nicholas, RS and Altmann, DM and Boyton, RJ},
doi = {10.1111/imm.12012.},
journal = {Immunology},
pages = {317--325},
title = {Increased HLA-E expression in white matter lesions in multiple sclerosis.},
url = {http://dx.doi.org/10.1111/imm.12012.},
volume = {137},
year = {2012}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - AbstractThe molecular mechanisms underpinning central nervous system (CNS) damage in multiple sclerosis (MS) are complex and it is widely accepted that there is an autoimmune component. Both adaptive and innate immune effector mechanisms are believed to contribute to tissue disease aetiology. HLA-E is a non-classical MHC class Ib molecule that acts as the ligand for the NKG2A inhibitory receptor present on natural killer (NK) and CD8(+) cells. Peptide binding and stabilisation of HLA-E is often considered to signal infection or cell stress. Here we examine the up-regulation of HLA-E in MS brain tissue. Expression is significantly increased in white matter lesions in the brain of MS patients compared to white matter of neurologically healthy controls. Furthermore, using quantitative immunohistochemistry and confocal microscopy, we show increased HLA-E protein expression in endothelial cells of active MS lesions. Non-inflammatory chronic lesions express significantly less HLA-E protein, comparable to levels found in white matter from controls. Increased HLA-E protein levels were associated with higher scores of inflammation. These results suggest the potential for an effect in CNS pathogenesis from HLA-E modulation in stressed tissue. Co-localisation with infiltrating CD8(+) cells implicates a possible role for HLA-E restricted regulatory CD8(+) cells, as has been proposed in other autoimmune diseases.
AU - Durrenberger,PF
AU - Webb,LV
AU - Sim,MJ
AU - Nicholas,RS
AU - Altmann,DM
AU - Boyton,RJ
DO - 10.1111/imm.12012.
EP - 325
PY - 2012///
SN - 0019-2805
SP - 317
TI - Increased HLA-E expression in white matter lesions in multiple sclerosis.
T2 - Immunology
UR - http://dx.doi.org/10.1111/imm.12012.
VL - 137
ER -