Anti‐LGI1 encephalitis is associated with unique HLA subtypes
Objective Autoimmune encephalitis (AE), represented by anti–leucine‐rich glioma‐inactivated 1 (anti‐LGI1) and anti–N‐methyl‐D‐aspartate receptor (anti‐NMDAR) encephalitis, has increasing clinical significance based on recent discoveries of neuronal autoantibodies. However, its immunopathogenesis is...
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Published in | Annals of neurology Vol. 81; no. 2; pp. 183 - 192 |
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Main Authors | , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.02.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Objective
Autoimmune encephalitis (AE), represented by anti–leucine‐rich glioma‐inactivated 1 (anti‐LGI1) and anti–N‐methyl‐D‐aspartate receptor (anti‐NMDAR) encephalitis, has increasing clinical significance based on recent discoveries of neuronal autoantibodies. However, its immunopathogenesis is not fully understood. Here, we investigated whether AE is associated with the human leukocyte antigen (HLA) subtypes.
Methods
We compared the HLA genotypes of 11 anti‐LGI1 and 17 anti‐NMDAR encephalitis patients to the control groups, which consisted of 210 epilepsy patients and 485 healthy Koreans.
Results
Anti‐LGI1 encephalitis was associated with the DRB1*07:01–DQB1*02:02 haplotype (10 patients; 91%) in HLA class II genes, as well as with B*44:03 (8 patients; 73%) and C*07:06 (7 patients; 64%) in the HLA class I region. The prevalence of these alleles in anti‐LGI1 encephalitis was significantly higher than that in the epilepsy controls or healthy controls. By contrast, anti‐NMDAR encephalitis was not associated with HLA genotypes. Additional analysis using HLA‐peptide binding prediction algorithms and computational docking underpinned the close relationship.
Interpretation
This finding suggests that most anti‐LGI1 encephalitis develops in a population with specific HLA subtypes, providing insight into a novel disease mechanism. Ann Neurol 2017;81:183–192 |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0364-5134 1531-8249 |
DOI: | 10.1002/ana.24860 |