Kate Attfield

Junior Principal Investigator

Multiple sclerosis (MS) is the most common, chronic disabling neurological condition in young adults, afflicting more than 2.5 million people worldwide. Genome-wide association studies (GWAS) have identified more than 200 risk loci as contributing to disease susceptibility. However, the clinical utility of this data ultimately requires functional translation to identify cell types or pathways that are perturbed by these variants and to understand the role that exogenous triggers, which activate and drive the disease. Our research aims to unravel this complexity using an array of experimental platforms and to integrate and complement our findings with clinical data.

Recent publications

Structural and regulatory diversity shape HLA-C protein expression levels.
Journal article

Kaur G. et al, (2017), Nat Commun, 8
Resolving TYK2 locus genotype-to-phenotype differences in autoimmunity.
Journal article

Dendrou CA. et al, (2016), Sci Transl Med, 8
Multiple sclerosis: Molecular mimicry of an antimyelin HLA class I restricted T-cell receptor.
Journal article

Rühl G. et al, (2016), Neurol Neuroimmunol Neuroinflamm, 3
Class II HLA interactions modulate genetic risk for multiple sclerosis.
Journal article

Moutsianas L. et al, (2015), Nat Genet, 47, 1107 - 1113
CD8⁺ MAIT cells infiltrate into the CNS and alterations in their blood frequencies correlate with IL-18 serum levels in multiple sclerosis.
Journal article

Willing A. et al, (2014), Eur J Immunol, 44, 3119 - 3128

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