November 1992
Volume 33, Issue 12
Free
Articles  |   November 1992
Human leukocyte antigen serologic and DNA typing of Behçet's disease and its primary association with B51.
Author Affiliations
  • N Mizuki
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • H Inoko
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • N Mizuki
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • H Tanaka
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • J Kera
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • K Tsuiji
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
  • S Ohno
    Department of Ophthalmology, Yokohama City University School of Medicine, Japan.
Investigative Ophthalmology & Visual Science November 1992, Vol.33, 3332-3340. doi:
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    • Get Citation

      N Mizuki, H Inoko, N Mizuki, H Tanaka, J Kera, K Tsuiji, S Ohno; Human leukocyte antigen serologic and DNA typing of Behçet's disease and its primary association with B51.. Invest. Ophthalmol. Vis. Sci. 1992;33(12):3332-3340.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Ninety Japanese patients with Behçet's disease (BD) were typed for human leukocyte antigen (HLA)-DRB1, -DQA1-, -DQB1, and -DPB1 alleles by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and for HLA-A, -B, -C, -DR, and -DQ antigens by conventional serologic typing. Serologic HLA typing showed a remarkably significant increase of HLA-B51 and a significant decrease of HLA-DQw1 in the patients with BD, especially those with ocular lesions including complete type, as compared with the control group (for B51, chi-squared = 46.75, P corrected < 0.001, relative risk [RR] = 7.9; for DQw1, chi-squared = 12.10, P corrected < 0.01, RR = 0.4). By PCR-RFLP genotyping, no significant difference was revealed in any class II alleles between the patient and the control groups in the corrected P value test, but P value analysis showed the significantly high frequency of DRB1*0802 and the significantly low frequencies of DQA1*0103, DQB1*0601, and DQB1*0501. No significant difference was observed in any DPB1 alleles by either P value analysis. These results indicated that the primary and primordial gene(s) responsible for the susceptibility to BD, especially related to ocular lesions, were not located in the HLA class II gene region but were in or very close to the HLA-B locus in the class I region. They also suggested the possibility that BD was a symptom complex associated with some independent diseases.

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