Experimental immune mediated arthritis in rhesus monkeys. A model for human rheumatoid arthritis?

The induction of experimental arthritis in rhesus monkeys was studied by intradermal immunization of bovine type II collagen and antigens derived from Mycobacterium tuberculosis, Streptococcus pyogenes, and Eubacterium aerofaciens. The tested bacterial antigens proved to be not arthrogenic. Bovine type II collagen induced clinical arthritis in 50% of the rhesus monkeys.

Immune complex formation between IgM rheumatoid factor and IgG generated by hyaluronic acid.

Immunoglobulin inclusions are regularly detected in granulocytes obtained from the synovial fluid of rheumatoid arthritis (RA) patients. In contrast, granulocytes isolated from the blood of the same patients usually contain no immunoglobulin inclusions. Using the indirect granulocyte phagocytosis test (IGPT), we obtained evidence that this discrepancy can be explained by the finding that hyaluronic acid (HA), a component of synovial fluid, increases the avidity of rheumatoid factor (RF), resulting in the formation of IgG-IgM-RF complexes.

Circulating immune complexes and rheumatoid arthritis: the induction of immune complex formation between rheumatoid factor and IgG by polyethylene glycol.

Circulating immune complexes (CIC) as detected by the C1q binding assay (C1qBA) in sera from patients with rheumatoid arthritis (RA) were not demonstrable in these sera with the indirect granulocyte phagocytosis test (IGPT). This discrepancy could be explained by the finding that polyethylene glycol (PEG), used in the C1qBA, enhanced the binding of rheumatoid factor IgM (RFIgM) and IgG resulting in immune complex (IC) formation. The addition of PEG to RA sera and subsequent testing of these sera in the IGPT revealed increased uptake of IC by these cells, dependent on the PEG dose.

Binding of anti-DNA antibodies to glomerular heparan sulfate: a new clue for the pathogenesis of SLE nephritis?

Antibodies against heparan sulfate (HS) were detected in sera from patients with active systemic lupus erythematosus (SLE) and in sera from MRL/l mice with a spontaneous SLE-like disease. By inhibition studies it was shown that this reactivity towards HS was due to cross-reactivity of anti-DNA antibodies. Immunoglobulin eluted from human and mouse kidneys with diffuse proliferative SLE glomerulonephritis also bound to HS.

Effects of cyclosporin A on autoimmune disease in MRL/1 and BXSB mice.

MRL/1 and BXSB mice were treated daily with cyclosporin A (CyA) in an oral dose of 25 mg/kg body weight. With this dose, blood levels within the therapeutic range were obtained. In normal mice CyA in this dose significantly prolonged the survival of an H-2 incompatible skin graft, and suppressed delayed-type hypersensitivity (DTH).