The functional MICA-129 polymorphism is associated with skin but not joint manifestations of psoriatic disease independently of HLA-B and HLA-C

• Published in: Tissue antigens Vol. 82; no. 1; pp. 43 - 47
• Main Authors: Pollock, R. A., Chandran, V., Pellett, F. J., Thavaneswaran, A., Eder, L., Barrett, J., Rahman, P., Farewell, V., Gladman, D. D.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.07.2013
• Subjects: Adult; Amino acids; Case-Control Studies; Demography; Female; Gene Frequency - genetics; Genetic Predisposition to Disease; Histocompatibility Antigens Class I - genetics; HLA-B; HLA-B Antigens; HLA-C; HLA-C Antigens - immunology; Homozygote; Humans; Joints - pathology; Logistic Models; major histocompatibility complex class I chain-related gene A; Male; MICA-129; Multivariate Analysis; Polymorphism, Single Nucleotide - genetics; psoriasis; Psoriasis - genetics; Psoriasis - immunology; psoriatic arthritis; Skin - pathology
• ISSN: 0001-2815; 1399-0039
• DOI: 10.1111/tan.12126

A methionine/valine polymorphism at amino acid 129 of the major histocompatibility complex class I chain‐related gene A (MICA‐129) categorizes alleles into strong and weak binders of the natural killer (NK) and T‐cell receptor NKG2D. We investigated whether MICA‐129 is differentially associated with skin and joint manifestations of psoriatic disease (PsD) independently of human leukocyte antigen (HLA)‐C and HLA‐B in patients and controls from Toronto and St. John's. The MICA‐129 methionine (Met) allele, particularly Met/Met homozygosity, was strongly associated with both cutaneous psoriasis (PsC) and psoriatic arthritis (PsA) independently of HLA‐B and HLA‐C in Toronto patients, and was also associated with PsA in St. John's patients, but with no additional effect of Met/Met homozygosity. No association remained after adjustment for HLA alleles in St. John's patients. MICA‐129 was not associated with PsA when compared with PsC. We conclude that MICA‐129 is a marker of skin manifestations of PsD that is independent of HLA class I in Toronto patients.