1. Killer Cell Immunoglobulin-Like Receptor Haplotype B Modulates Susceptibility to EBV-Associated Classic Hodgkin Lymphoma
- Author
-
Peijia Jiang, Ilja M. Nolte, Bouke G. Hepkema, Marijke Stulp, Anke van den Berg, Arjan Diepstra, Life Course Epidemiology (LCE), Translational Immunology Groningen (TRIGR), and Stem Cell Aging Leukemia and Lymphoma (SALL)
- Subjects
Adult ,Male ,HLA CLASS-I ,MECHANISM ,Epstein-Barr Virus Infections ,Herpesvirus 4, Human ,Adolescent ,IMPACT ,Immunology ,PATHOGENESIS ,DIVERSITY ,NK cells ,susceptibility ,DISEASE ,Young Adult ,MOLECULES ,Receptors, KIR ,EBV ,hemic and lymphatic diseases ,Humans ,Immunology and Allergy ,EPSTEIN-BARR-VIRUS ,Aged ,Aged, 80 and over ,B-Lymphocytes ,HLA class I ,Middle Aged ,RC581-607 ,Hodgkin Disease ,KIR ,Haplotypes ,Receptors, KIR2DL2 ,Female ,CHL ,Immunologic diseases. Allergy ,INFECTIOUS-MONONUCLEOSIS - Abstract
Tumor cells of classic Hodgkin lymphoma (cHL) are derived from antigen presenting B cells that are infected by Epstein Barr virus (EBV) in ~30% of patients. Polymorphic Killer cell immunoglobulin-like receptors (KIRs) expressed on NK cells interact with human leukocyte antigen (HLA) class I and play a key role in immune surveillance against virally infected cells and tumor cells. We investigated the effect of KIR types on cHL susceptibility overall (n=211) and in EBV-stratified subgroups using the Dutch GoNL cohort as controls (n=498). The frequency of the KIR haplotype B subgroup was significantly different between EBV+ and EBV− cHL patients (62% vs. 77%, p=0.04) and this difference was more pronounced in nodular sclerosis (NS) cHL (49% vs. 79%, p=0.0003). The frequency of KIR haplotype B subgroup was significantly lower in EBV+ NS cHL compared to controls (49% vs. 67%, p=0.01). Analyses of known KIR – HLA interaction pairs revealed lower carrier frequencies of KIR2DS2 – HLA-C1 (29% vs. 46%, p=0.03) and KIR2DL2 – HLA-C1 (29% vs. 45%, p=0.04) in EBV+ NS cHL patients compared to controls. Carriers of the KIR haplotype B subgroup are less likely to develop EBV+ NS cHL, probably because of a more efficient control over EBV-infected B cells.
- Published
- 2022