• rheumatoid arthritis;
  • cytophilic IgA;
  • T cells with Fcα receptors


Autoimmunity may be due to augmentation of immune responses by human CD8 cells which bind the lectin Vicia villosa (VV). We have investigated T cells in rheumatoid arthritis (RA) by double immunofluorescence flow cytometry, in order to assess VV-binding CD8 and CD4 cells from the peripheral blood and synovial fluid. A significant increase in CD8+ VV adherent (P<0.0001) and CD4+ VV adherent cells (P <0.001) was found in synovial fluid, as compared with peripheral blood from patients with RA. A significant increase in VV-binding CD8+ or CD4+ cells was, however, not found in the blood of patients with RA, as compared with controls. We suggest that the lack of VV-binding T cells separated from blood, in contrast to those from synovial fluid, may be due to an inhibiting agent expressing N-acetyl d-galactosamine. Indeed, IgA1 is rich in N-acetyl d-galactosamine, it inhibits VV binding to T cells and is significantly bound to CD8 cells (P<0.001). The IgA1 was then characterized and in about half the patients J chains and secretory component was found, suggesting that the IgA1 is of the polymeric and secretory variety. IgA bound to the T cells engaged the Fcα receptors and a significant decrease in the Fcα receptors was found in CD8 cells (P<0.000l) and CD4 cells (P<0.0l). Desorption studies were then carried out on CD8 and CD4 cells which showed that a loss of cell-bound IgA1 was associated with an increase in VV binding. Conversely, adsorption of IgA to T cells was associated with a loss in VV binding. The results suggest that the failure of VV binding to CD8+ andCD4+ cells from peripheral blood of patients with RA can be ascribed to cell-bound IgA 1. Cytophilic IgA1 may inhibit the function of CD8+ VV binding cells, thereby preventing augmentation of the systemic immune response, consistent with the lack of extra-articular disease in these patients with RA.