The influence of human leukocyte antigen-DRB1*15:01 and its interaction with smoking in MS development is dependent on DQA1*01:01 status.


Journal

Multiple sclerosis (Houndmills, Basingstoke, England)
ISSN: 1477-0970
Titre abrégé: Mult Scler
Pays: England
ID NLM: 9509185

Informations de publication

Date de publication:
11 2020
Historique:
pubmed: 2 10 2019
medline: 25 9 2021
entrez: 2 10 2019
Statut: ppublish

Résumé

HLA-DRB1*15:01, absence of HLA-A*02:01, and smoking interact to increase multiple sclerosis (MS) risk. To analyze whether MS-associated human leukocyte antigen (HLA) alleles, apart from DRB1*15:01 and absence of A*02:01, interact with smoking in MS development, and to explore whether the established HLA-smoking interaction is affected by the DQA1*01:01 allele, which confers a protective effect only in the presence of DRB1*15:01. In two Swedish population-based case-control studies (5838 cases, 5412 controls), subjects with different genotypes and smoking habits were compared regarding MS risk, by calculating odds ratios with 95% confidence intervals employing logistic regression. Interaction on the additive scale between different genotypes and smoking was evaluated. The DRB1*08:01 allele interacted with smoking to increase MS risk. The interaction between DRB1*15:01 and both the absence of A*02:01 and smoking was confined to DQA1*01:01 negative subjects, whereas no interactions occurred among DQA1*01:01 positive subjects. Multifaceted interactions take place between different class II alleles and smoking in MS development. The influence of DRB1*15:01 and its interaction with the absence of A*02:01 and smoking is dependent on DQA1*01:01 status which may be due to differences in the responding T-cell repertoires.

Sections du résumé

BACKGROUND
HLA-DRB1*15:01, absence of HLA-A*02:01, and smoking interact to increase multiple sclerosis (MS) risk.
OBJECTIVE
To analyze whether MS-associated human leukocyte antigen (HLA) alleles, apart from DRB1*15:01 and absence of A*02:01, interact with smoking in MS development, and to explore whether the established HLA-smoking interaction is affected by the DQA1*01:01 allele, which confers a protective effect only in the presence of DRB1*15:01.
METHODS
In two Swedish population-based case-control studies (5838 cases, 5412 controls), subjects with different genotypes and smoking habits were compared regarding MS risk, by calculating odds ratios with 95% confidence intervals employing logistic regression. Interaction on the additive scale between different genotypes and smoking was evaluated.
RESULTS
The DRB1*08:01 allele interacted with smoking to increase MS risk. The interaction between DRB1*15:01 and both the absence of A*02:01 and smoking was confined to DQA1*01:01 negative subjects, whereas no interactions occurred among DQA1*01:01 positive subjects.
CONCLUSION
Multifaceted interactions take place between different class II alleles and smoking in MS development. The influence of DRB1*15:01 and its interaction with the absence of A*02:01 and smoking is dependent on DQA1*01:01 status which may be due to differences in the responding T-cell repertoires.

Identifiants

pubmed: 31573825
doi: 10.1177/1352458519877685
doi:

Substances chimiques

HLA Antigens 0
HLA-DQ beta-Chains 0
HLA-DRB1 Chains 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1638-1646

Auteurs

Anna Karin Hedström (AK)

Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.

Ola Hössjer (O)

Department of Mathematical Statistics, Stockholm University, Stockholm, Sweden.

Jan Hillert (J)

Department of Clinical Neuroscience and Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

Pernilla Stridh (P)

Department of Clinical Neuroscience and Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

Ingrid Kockum (I)

Department of Clinical Neuroscience and Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

Tomas Olsson (T)

Department of Clinical Neuroscience and Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

Lars Alfredsson (L)

Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.

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Classifications MeSH