Identification and characterization of IgA and Vicia villosa-binding T cell subsets in rheumatoid arthritis

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Abstract
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+ VV adherent cells (P + 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 (PPP+ 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.

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