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MICA and NKG2D variants as risk factors in spondyloarthritis: a case-control study

Marie Fechtenbaum1,2, Judith Desoutter3, Gauthier Delvallez3

  • 1Department of Rheumatology, Amiens University Medical Center, Amiens, France. marie.fechtenbaum@wanadoo.fr.

Genes and Immunity
|September 5, 2018
PubMed

Insights

Genetic variations in MICA and NKC3 influence natural killer cell activity and are associated with spondyloarthritis. Specific MICA alleles and NKC3 genotypes linked to lower NK cell cytotoxicity show a significant association with these inflammatory conditions.

Area of Science:

  • Immunogenetics
  • Rheumatology
  • Molecular Biology

Background:

  • The Major Histocompatibility Complex class I polypeptide-related sequence A (MICA) glycoprotein interacts with the Natural Killer Group 2D (NKG2D) receptor, influencing immune responses.
  • Polymorphisms in MICA and NKG2D receptor genes, such as MICA-129 and NKC3, affect MICA-NKG2D binding affinity and natural killer (NK) cell cytotoxic activity.

Purpose of the Study:

  • To investigate the association between MICA and NKC3 gene polymorphisms and spondyloarthritis, including ankylosing spondylitis and psoriatic arthritis.
  • To determine if specific MICA or NKC3 variants correlate with disease susceptibility or specific subtypes of spondyloarthritis.

Main Methods:

  • Case-control study comparing 162 spondyloarthritis patients (including ankylosing spondylitis and psoriatic arthritis) with 124 healthy controls.
  • Genotyping for MICA-129 (methionine/valine), MICA A5.1 allele, and NKG2D polymorphisms (NKC3 and NKC4).
  • Statistical analysis, including odds ratios (OR) and adjusted ORs for HLA-B*27, to assess genetic associations.

Main Results:

  • The MICA-129 methionine allele was more frequent in spondyloarthritis patients (OR=4.84).
  • MICA-129 val/val, MICA A5.1, and NKC3 C/C variants were less frequent, suggesting a protective effect (ORs ranging from 0.15 to 0.24).
  • After adjusting for HLA-B*27, only NKC3 C/C remained significantly associated with spondyloarthritis (adjusted OR=0.14). Homozygosity for MICA A5.1 and NKC3 C/C and MICA-129 val/val were linked to specific subtypes.

Conclusions:

  • MICA and NKC3 polymorphisms, particularly those associated with reduced NK cell cytotoxic activity, are genetically linked to spondyloarthritis.
  • Specific genotypes like NKC3 C/C and MICA-129 val/val may confer protection against or be associated with specific subtypes of spondyloarthritis.

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