Association of MICA-129 polymorphism with nasopharyngeal cancer risk in a Tunisian population

• Published in: Human immunology Vol. 70; no. 1; pp. 45 - 48
• Main Authors: Douik, Hayet, Chaaben, Arij Ben, Romdhane, Neila Attia, Ben Romdhane, Habiba, Mamoghli, Tesnim, Fortier, Catherine, Boukouaci, Wahid, Harzallah, Latifa, Ghanem, Abderraouf, Gritli, Said, Makni, Mohamed, Charron, Dominique, Krishnamoorthy, Rajagopal, Guemira, Fethi, Tamouza, Ryad
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 2009
• Subjects: Adult; Aged; Allergy and Immunology; Amino Acid Substitution; Cohort Studies; Female; Genetic Predisposition to Disease; Histocompatibility Antigens Class I - genetics; Humans; Linkage Disequilibrium; Male; MICA gene polymorphism; Middle Aged; Nasopharyngeal cancer; Nasopharyngeal Neoplasms - genetics; NK Cell Lectin-Like Receptor Subfamily K - metabolism; Polymorphism, Genetic; Risk; Tunisia; Tunisia; MICA gene polymorphism; Tunisia; Nasopharyngeal cancer
• ISSN: 0198-8859; 1879-1166
• DOI: 10.1016/j.humimm.2008.10.008

Abstract Major histocompatibility complex (MHC) class I chain–related A (MICA) molecules mediate natural killer (NK) cell activation and T lymphocyte co-stimulation. A polymorphic methionine (met) to valine (val) variation at amino acid position 129 of the α2 heavy chain domain is in linkage disequilibrium with other allelic changes and seems to categorize MICA alleles into strong and weak binder of NKG2D receptor and thereby to influence effector cell function. We investigated here whether MICA-129 dimorphism is associated with susceptibility to/or resistance against developing nasopharyngeal cancer (NPC). DNA from 130 NPC patients and 180 healthy individuals from Tunisia were genotyped for MICA-129 variation. We found a higher frequency of MICA-129 val/val genotype in patients than in controls (corrected p value = 0.02) that could suggest a tumor escape mechanism because of failure to activate NK cells by MICA-129 val allele or absence of NK cell activation because of absence of MICA-129 met allele in individuals otherwise predisposed to viral/environmental factors.