Sera from 29 children with acute Henoch-Schönlein purpura were tested for IgA antineutrophil cytoplasmic antibody (ANCA) and for IgA rheumatoid factor (RF). All sera were negative for IgA ANCA by indirect immunofluorescence, but 13 of 29 patients had weakly positive results for IgA ANCA when tested using an enzyme immunoassay. Sixteen of 29 children were IgA RF seropositive. IgA RF seropositive patients had significantly higher titers of IgA ANCA as compared with IgA RF seronegative patients (p = 0.0002). Indeed, of the 16 patients who were IgA RF seropositive, 13 also had positive tests for IgA ANCA, while none of the IgA RF seronegative patients had positive tests for IgA ANCA (p = 0.00001). Removal of IgA RF from eight sera by adsorption with immobilized IgG produced comparable reductions in the titers of both IgA RF and IgA ANCA. We conclude that IgA ANCA is not an important serologic marker in Henoch-Schönlein purpura, but the presence of serum IgA RF may produce weak false-positive results for IgA ANCA in some patients.

We have produced experimental autoimmune glomerulonephritis (EAG) in histocompatible SC chickens by immunization with different types of glomerular antigen. The development of EAG was time, but not antigen, dependent. Transfer of mononuclear cells from spleens and kidneys of nephritic animals resulted in EAG in naive recipients. Transferred EAG developed earlier than in immunized donors and was not associated with circulating or bound anti-GBM antibodies. Control recipients did not develop disease from control cells alone, soluble antigen, or antigen plus control cells. The cells which transferred EAG appeared morphologically by light and electron microscopy to be lymphocytes, sedimented as lymphocytes, were positive with anti-serum to thymocytes but negative with anti-bursa anti-serum, stained as T-cells with monoclonal antibodies and underwent blast transformation in response to mitogen and GBM antigen. Other organ specific diseases have been transferred by cells alone; to our knowledge this is the first description of glomerulonephritis transferred by cells alone. This new pathogenetic process may play an important role in the development of glomerulonephritis in other animal models as well as in humans.

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