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- Title
Fc?R expression on NK cells influences disease severity in rheumatoid arthritis.
- Authors
Stewart-Akers, A. M.; Cunningham, A.; Wasko, M. C.; Morel, P. A.
- Abstract
Rheumatoid arthritis (RA) is associated with autoantibodies, the best known of which is rheumatoid factor (RF). RF/IgG complexes interact with Fc?R on the surface of neutrophils, NK cells and monocyte/macrophages. We have analyzed the expression pattern and allelic polymorphisms of three Fc?R genes (Fc?RIIA, Fc?RIIC and Fc?RIIIA) in a large sample of RA patients and normal donors. We have found that the level of Fc?R (CD16 and CD32) expression on NK cells is lower in RA patients than in normal individuals. Genotypic analysis demonstrated that the CD32 isoform expressed by the majority of RA patients was not the activating Fc?RIIc1 isoform, commonly seen in normal individuals, but rather the inhibitory Fc?RIIb isoform. The combination of the Fc?RIIIA-176F allele with a lack of CD32 expression in NK cells appeared to be characteristic of RA subjects with aggressive disease. Since Fc?RII and Fc?RIIIA are predominantly expressed by NK cells, these data further suggest that Fc?R-mediated activation of NK cells could be a disease-determining factor in RA patients.Genes and Immunity (2004) 5, 521-529. doi:10.1038/sj.gene.6364121 Published online 26 August 2004
- Subjects
KILLER cells; RHEUMATOID arthritis; GENETIC polymorphisms; RHEUMATOID factor; MONOCYTES; GENETICS
- Publication
Genes & Immunity, 2004, Vol 5, Issue 7, p521
- ISSN
1466-4879
- Publication type
Article
- DOI
10.1038/sj.gene.6364121