alexa HLA-DRB1* Allele Frequencies in Pediatric, Adolescent and Adult-Onset Multiple Sclerosis Patients, in a Hellenic Sample. Evidence for New and Established Associations
ISSN: 2376-0389

Journal of Multiple Sclerosis
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Research Article

HLA-DRB1* Allele Frequencies in Pediatric, Adolescent and Adult-Onset Multiple Sclerosis Patients, in a Hellenic Sample. Evidence for New and Established Associations

Maria C Anagnostouli1,2*, Argyro Manouseli1,3, Artemios K Artemiadis1, Serafeim Katsavos1, Constantina Fillipopoulou1,3, Sotirios Youroukos1, Spyros Efthimiopoulos3 and Ilias Doxiadis4

1 Immunogenetics Laboratory, 1st Department of Neurology, Aeginition Hospital, Medical School of National and Kapodistrian University of Athens, Athens, Greece

2 1st Department of Neurology, Aeginition Hospital, Medical School of National and Kapodistrian University of Athens, Athens, Greece

3 Department of Biology, Division of Animal and Human Physiology of National and Kapodistrian University of Athens, Athens, Greece

4 Department of Immunohaematology and Blood Transfusion, University Hospital, Leiden, The Netherlands

Corresponding Author:
Maria C Anagnostouli
Assistant Professor of Neurology and Director of Immunogenetics Laboratory
1st Department of Neurology
Aeginition Hospital, National and Kapodistrian University of Athens
72-74 Vas. Sophias Avenue, 11528 Athens, Hellas
Tel: +30210728 9165
Fax: +30210685 2913
E-Mail: [email protected]

Received date: April 1, 2014; Accepted date: May 22, 2014; Published date: May 26, 2014

Citation: Anagnostouli MC, Manouseli A, Artemiadis AK, Katsavos S, Fillipopoulou C et al. (2014) HLA-DRB1* Allele Frequencies in Pediatric, Adolescent and Adult-Onset Multiple Sclerosis Patients, in a Hellenic Sample. Evidence for New and Established Associations. J Mult Scler 1:104. doi:10.4172/2376-0389.1000104

Copyright: © 2014 Anagnostouli MC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Studies in many populations consistently have showed that the human leukocyte antigens (HLA) and especially the DRB1*15 allele has by far the strongest genetic association with multiple sclerosis (MS). The aim of this study was to investigate the role of HLA-DRB1* alleles in MS risk/resistance and onset. A sample of 165 Hellenic MS patients (18 with pediatric-, 24 with adolescent- and 123 with adult-onset MS) and 107 healthy volunteers were examined with molecular techniques. Comparisons were made according to the Benjamini-Yekutieli method for p value correction. Both adult-onset MS patients and early-onset MS patients (age at onset below 20 years-old) had a significantly higher frequency of the DRB1*15 allele and a significantly lower frequency of the DRB1*11 allele compared to controls. For the early-onset vs. healthy group comparison, subgroup analyses revealed that both the pediatric- and the adolescent-onset MS groups contributed to the aforementioned DRB1*15 significant difference, while the DRB1*11 difference was ascribed solely to the adolescent-MS onset vs. healthy group comparison. Within MS patients comparisons revealed that early-onset MS patients had a tendency for higher DRB1*03 allele and a lower DRB1*16 allele frequency frequencies compared to adult-onset MS patients, although both non-significant. Notably, pediatric-onset MS patients showed complete absence of the DRB1*16 allele, along with a non-significant tendency for higher DRB1*15 allele frequency relative to the adult-onset group. Finally, the adolescent-onset MS group was presented with a lower DRB1*11 allele frequencies compared both to the pediatric- and the adult-onset MS group. Our findings confirm previous studies on the role of HLA-DRB1* in MS. New findings that need to be confirmed by further studies are the pathogenetic role of DRB1*03 for early-onset MS and the putative protective role of the DRB1*16 allele in the pediatric-onset MS.

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