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¹ Basic Research Program, Laboratory of Genomic Diversity, Science Applications International Corporation-Frederick, Inc., National Cancer Institute, Frederick, MD 21702
² Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20892
³ Proyecto Epidemiologico Guanacaste, 301-6151, San Jose, Costa Rica
⁴ Division of Gynecologic Pathology, Johns Hopkins Medical Institutes, Baltimore, MD 21231
⁵ Milton S. Hershey Medical Center, Hershey, PA 17033
⁶ Yale University School of Medicine, New Haven, CT 06520
⁷ Kaiser Permanente Center for Health Research, Portland, OR 97227

CORRESPONDENCE Mary Carrington: carringt{at}ncifcrf.gov

Killer immunoglobulin-like receptor (KIR) recognition of specific human histocompatibility leukocyte antigen (HLA) class I allotypes contributes to the array of receptor–ligand interactions that determine natural killer (NK) cell response to its target. Contrasting genetic effects of KIR/HLA combinations have been observed in infectious and autoimmune diseases, where genotypes associated with NK cell activation seem to be protective or to confer susceptibility, respectively. We show here that combinations of KIR and HLA loci also affect the risk of developing cervical neoplasia. Specific inhibitory KIR/HLA ligand pairs decrease the risk of developing neoplasia, whereas the presence of the activating receptor KIR3DS1 results in increased risk of disease, particularly when the protective inhibitory combinations are missing. These data suggest a continuum of resistance conferred by NK cell inhibition to susceptibility involving NK cell activation in the development of cervical neoplasia and underscore the pervasive influence of KIR/HLA genetic variation in human disease pathogenesis.

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