Imperial College London

ProfessorRosemaryBoyton

Faculty of MedicineDepartment of Infectious Disease

Professor of Immunology and Respiratory Medicine
 
 
 
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Contact

 

r.boyton

 
 
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Location

 

8N22Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Reynolds:2015:10.1186/s12974-015-0313-9,
author = {Reynolds, CJ and Sim, MJ and Quigley, KJ and Altmann, DM and Boyton, RJ},
doi = {10.1186/s12974-015-0313-9},
journal = {Journal of Neuroinflammation},
title = {Autoantigen cross-reactive environmental antigen can trigger multiple sclerosis-like disease.},
url = {http://dx.doi.org/10.1186/s12974-015-0313-9},
volume = {12},
year = {2015}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - BACKGROUND: Multiple sclerosis is generally considered an autoimmune disease resulting from interaction between predisposing genes and environmental factors, together allowing immunological self-tolerance to be compromised. The precise nature of the environmental inputs has been elusive, infectious agents having received considerable attention. A recent study generated an algorithm predicting naturally occurring T cell receptor (TCR) ligands from the proteome database. Taking the example of a multiple sclerosis patient-derived anti-myelin TCR, the study identified a number of stimulatory, cross-reactive peptide sequences from environmental and human antigens. Having previously generated a spontaneous multiple sclerosis (MS) model through expression of this TCR, we asked whether any of these could indeed function in vivo to trigger CNS disease by cross-reactive activation. FINDINGS: A number of myelin epitope cross-reactive epitopes could stimulate T cell immunity in this MS anti-myelin TCR transgenic model. Two of the most stimulatory of these 'environmental' epitopes, from Dictyostyelium slime mold and from Emiliania huxleyi, were tested for the ability to induce MS-like disease in the transgenics. We found that immunization with cross-reactive peptide from Dictyostyelium slime mold (but not from E. huxleyi) induces severe disease. CONCLUSIONS: These specific environmental epitopes are unlikely to be common triggers of MS, but this study suggests that our search for the cross-reactivity triggers of autoimmune activation leading to MS should encompass epitopes not just from the 'infectome' but also from the full environmental 'exposome.'
AU - Reynolds,CJ
AU - Sim,MJ
AU - Quigley,KJ
AU - Altmann,DM
AU - Boyton,RJ
DO - 10.1186/s12974-015-0313-9
PY - 2015///
SN - 1742-2094
TI - Autoantigen cross-reactive environmental antigen can trigger multiple sclerosis-like disease.
T2 - Journal of Neuroinflammation
UR - http://dx.doi.org/10.1186/s12974-015-0313-9
UR - http://hdl.handle.net/10044/1/23372
VL - 12
ER -