Although F11 receptor (F11R), also named junctional adhesion molecular A (JAM-A), participates in leukocyte migration, its role in autoimmune diseases has not been specifically disclosed. In this study, we examined the association of F11R expression with the development and clinical manifestations of rheumatoid arthritis (RA).
RNA from peripheral blood mononuclear cells (PBMCs) and DNA from the peripheral blood in RA patients and a healthy control group were extracted. F11R messenger RNA (mRNA) expression was determined by quantitative real-time polymerase chain reaction. The F11R polymorphisms were determined by the TaqMan genotyping assay.
There was more F11R mRNA expression in the PBMCs of RA patients than those of the control group (P = 0.018). In F11R promoter -688 A > C, C carriers have lower titers of the anticyclic citrullinated peptide (anti-CCP) antibodies (P = 0.002) and fewer positive rates of Schirmer's tests (P = 0.009). The effect is independent of the existence of HLA-DR4. Different genotypes in F11R promoter -688 A > C and -436 A > G do not lead to changes of the gene expression in RA patients.
RA patients have higher mRNA expression of F11R. In RA patients, F11R -688 C may be a protective factor for the development of anti-CCP antibodies and positive rates of Schirmer's tests.