| Rheumatoid arthritis (RA) is a common chronic inflammatory and autoimmune disorder of unknown etiology that to date has no known cause or cure. RA is characterized by synovial inflammation, proliferation and progressive joint destruction, and patients with high titers of IgA-type rheumatoid factor typically follow a more aggressive and destructive disease course. In the present study, the role of IgA in RA was evaluated by investigating whether RA fibroblast-like synoviocytes (FLS) expressed receptors for IgA. Immunofluorescent staining of RA and osteoarthritis (OA) FLS cell cultures showed that the IgA receptor FcalphaR (CD89) previously described in granulocytes was expressed on both types of FLS, but not in fibroblasts from uninflamed non-synovial tissue. All RA and OA FLS were tested for their ability to express mRNA for IgA receptors and FcgammaRIII via RT-PCR. DNA sequencing of the RT-PCR products confirmed FcalphaR and FcgammaRIII identity. While every RA and OA patient tested positive for both FcalphaR and FcgammaRIII, none expressed mRNA for the polymeric immunoglobulin receptor described in epithelial cells or the Fcalpha/muR in white blood cells. Immunohistochemistry on fresh frozen RA and OA tissue showed specific staining for FcalphaR predominantly in the intimal lining layer, confirming expression in vivo.; In conclusion, RA and OA FLS constitutively express the IgA receptor FcalphaR both in vitro and in vivo. While this work confirms the presence of the receptor on FLS cells, which have the ability to contribute to the powerful pro-inflammatory process that characterizes RA, further studies are required to define the role of FcalphaR in arthritis. |
