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HLA-A*02 is associated with a reduced risk and HLA-A*01 with an increased risk of developing EBVI Hodgkin lymphoma

Niens, M., Jarreft, R. F., Hepkema, B., Nolte, I. M., Diepstra, A., Platteel, M., Kouprie, N., Delury, C. P., Gallagher, A., Visser, L., Poppema, S., te Meerman, G. J. & Van den Berg, A. 1-Nov-2007 In : Blood. 110, 9, p. 3310-3315 6 p.

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  • HLA-A*02 is associated with a reduced risk and HLA-A*01 with an increased risk of developing EBV+ Hodgkin lymphoma

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DOI

Previous studies showed that the HLA class I region is associated with Epstein-Barr virus (EBV)-positive Hodgkin lymphoma (HL) and that HLA-A is the most likely candidate gene in this region. This suggests that antigenic presentation of EBV-derived peptides in the context of HLA-A is involved in the pathogenesis of EBV+ HL by precluding efficient immune responses. We genotyped exons 2 and 3, encoding the peptide-binding groove of HLA-A, for 32 single nucleotide polymorphisms in 70 patients with EBV+ HL, 31 patients with EBV- HL, and 59 control participants. HLA-A*O1 was significantly overrepresented and HLA-A*O2 was significantly underrepresented in patients with EBV+ HL versus controls and patients with EBV- HL. In addition, HLA-A*O2 status was determined by immunohistochemistry or HLA-A*O2-specific polymerase chain reaction (PCR) on 152 patients with EBV+ HL and 322 patients with EBV-HL. The percentage of HLA-A*O2(+) patients in the EBV+ HL group (35.5%) was significantly lower than in 6107 general control participants (53.0%) and the EBV- HL group (50.9%). Our results indicate that individuals carrying the HLA-A*O2 allele have a reduced risk of developing EBV+3 HL, while individuals carrying the HLA-A*O1 allele have an increased risk. It is known that HLA-A*O2 can present EBV-derived peptides and can evoke an effective immune response, which may explain the protective phenotype.

Original languageEnglish
Pages (from-to)3310-3315
Number of pages6
JournalBlood
Volume110
Issue number9
StatePublished - 1-Nov-2007

    Keywords

  • EPSTEIN-BARR-VIRUS, MAJOR HISTOCOMPATIBILITY COMPLEX, REED-STERNBERG CELLS, HLA-CLASS-I, INFECTED CELLS, DISEASE, PROTEIN, PHENOTYPE, EPITOPES, SEQUENCE

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