4.2 Article

The association of class IHLA alleles and antibody levels after a single dose of measles vaccine

期刊

HUMAN IMMUNOLOGY
卷 64, 期 1, 页码 103-109

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/S0198-8859(02)00741-3

关键词

Genes; MHC class I; measles vaccine; antibody formation

资金

  1. NCRR NIH HHS [M01-RR-00585-25] Funding Source: Medline
  2. NIAID NIH HHS [N01-AI-45240, R01-2AI-33144] Funding Source: Medline
  3. NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000585] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI033144, N01AI045240] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Despite the success of the current measles vaccine in controlling disease in industrialized countries, the importance of vaccine failure has become increasingly apparent. Our objective was to determine if associations exist between seronegativity after measles vaccination and class I human leukocyte antigen (HLA) alleles. We undertook a cross-sectional observational study in Rochester, Minnesota, with 242 school-age children previously recruited from a communitywide seroprevalence study. We studied two groups of subjects: 72 were seronegative (EIA less than or equal to0.8 after a single dose of measles vaccine) and 170 were sempositive (enzyme immunoassy [EIA] greater than or equal to1.0 after one dose). We used the resources of Mayo Clinic's tissue typing laboratory for serotyping class I HLA-A and HLA-B alleles via microlymphocytotoxicity assays. We found no statistically significant associations with class I HLA-A but did find associations with class I HLA-B, which includes alleles associated with seronegativity (138, 1313, and 1344) and those associated with sempositivity (137 and 1351). Elucidation of the specific peptide-HLA complex interactions that lead to varying or failed immune responses may provide fertile groundwork for improved vaccines that can overcome limitations of the current live, attenuated measles vaccine. (C) American Society for Histocompatibility and Immunogenetics, 2003. Published by Elsevier Science Inc.

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