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To evaluate the level of lymphocyte activation in reactive and rheumatoid arthritis, density gradient-isolated, synovial fluid mononuclear cells were stained with a panel of antisera directed at lymphocyte activation markers using an avidin-biotin-peroxidase complex (ABC) method. More specifically, we studied the expression of immune response-associated class II HLA antigen (Ia), of receptors for interleukin 2 (Tac) and transferrin (T9), as well as of gp 40/80 glycoprotein (4F2). Although Ia+ cells formed about 60% of all the synovial fluid mononuclear cells in both disease conditions, the proportion of Tac+ (33 +/- 4% vs 3 +/- 1%, P less than 0.001), T9+ (34 +/- 4% vs 5 +/- 2%, P less than 0.001), and 4F2+ (48 +/- 6% vs 3 +/- 2%, P less than 0.001) cells was high only in reactive arthritis. All the patients who had reactive arthritis followed a favourable clinical course during the 4-month-long prospective follow-up, whereas disease activity was stable in patients with rheumatoid arthritis. These findings suggest that the diseased joints in reactive arthritis are a site for an active, but normally down-regulated, cell-mediated immune response.

ABSTRACT. A patient with seronegative rheumatoid arthritis developed a nephrotic syndrome. Histological examination of renal biopsy disclosed moderate amyloidosis. Ultrastructurally the glomerular amyloid deposits were seen to be located both within the mesangium and subepithelially in the peripheral capillaries. The patient was treated with prednisone and cyclophosphamide for two years. The nephrotic syndrome remitted and a follow‐up biopsy showed almost total disappearance of Congo red positive amyloid substance. Electron microscopy showed abundant finely granular material but only small amounts of fibrillar amyloid in the mesangial regions and intramembranous lucent areas containing few amyloid fibrils but no subepithelial deposits in the peripheral capillaries. We conclude that the mesangial amyloid substance was degraded to granular material and that the subepithelial amyloid deposits were resolved by mechanisms similar to those involved in the resolution of subepithelial immune complex deposits, i.e. through slow washing out and incorporation into the basement membrane.

Clinical and serological findings of 16 patients with systemic lupus erythematosus (SLE) who had progressive cystic bone lesions were compared with a control group of 19 patients with SLE without radiological evidence of bone cysts. Central nervous system manifestations, synovitis, and other radiologically observed skeletal abnormalities were more prevalent in the patients with cysts than in the control group. Higher concentrations of C reactive protein, and a greater incidence of rheumatoid factor positivity were seen in the patients with cysts than in the control patients, but no other serological differences were found. It is suggested that patients with SLE with progressive cystic lesions form a subgroup of the syndrome characterised by an increased acute phase reaction.