Patients with Sjögren's syndrome (SS) display two sets of immunological abnormalities. B cells are oligoclonally activated, resulting in hypergammaglobulinaemia, elevated levels of circulating immune complexes (CIC) and non-organ specific autoantibodies. The cellular arm of the immune response is also involved, as shown by the predominance of activated T cells within the exocrine gland infiltrate. IgA could well bridge the gap between activated B cells and defective T cells and by doing so, play a pivotal role in the pathogenesis of SS. This interpretation is supported by the high proportion of IgA in immunoglobulin(Igl) production at the mucosal level. Additionally, IgA is the Igl class most dependent on T cell help. A number of studies over the past 15 years have reported high levels of serum and secretory IgA, IgA-rheumatoid factor and IgA-containing CIC. A correlation between disease activity and the latter abnormalities has recently been shown. There is, however, a need for longitudinal assessment of total IgA and IgA autoantibodies in order to further evaluate their role in the pathogenesis of the disease.