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Immunology |
Immunology Group, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester M20 4BX [E. J. D., P. L. S.]; Academic Unit of Obstetrics and Gynaecology, St. Marys Hospital, Manchester M13 0JH [E. J. D., H. C. K.]; Transplantation Laboratory, Manchester Clinic Building, Manchester Royal Infirmary, Manchester M13 9WL [J. A. D.]; and Division of Virology, Department of Pathology, University of Cambridge, Addenbrookes Hospital, Cambridge CB2 2QQ [J. C. S., P .J. W. B.], United Kingdom
Polymorphisms in human leukocyte antigen (HLA) genes have been implicated in the risk for developing human papillomavirus (HPV)-associated cervical neoplasia. By comparison with local cadaver controls typed for HLA class I (n = 946) and II (n = 144) antigens, HPV-16-positive high grade vulval intraepithelial neoplasia patients (n = 42) showed significantly different frequencies of HLA-A2 [odds ratio (OR), 2.1; confidence interval (CI), 1.43.9], HLA-B7 (OR, 2.6; CI, 1.44.7), HLA-DRB1*0101/02/04 (OR, 0.1; CI, 0.030.5), HLA-DRB1*11 (OR, 3.3; CI, 1.47.1), HLA-DRB1*13 (OR, 0), HLA-DQB1*05 (OR, 0.2; CI, 0.050.6), and HLA-DQB1*03032 (OR, 4.6; CI, 1.514.0). With the exception of HLA-B7 and HLA-DRB1*11, these significant differences were also seen comparative to local HPV-16-positive cervical carcinoma patients (n = 114), suggesting a specific immunogenetic contribution that is independent of HPV-16 infection in high-grade vulval intraepithelial neoplasia. Such factors are important to the development of HPV vaccines for treatment of cervical and vulval neoplasia.
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