Modification of NZB/NZW F1 Autoimmune Disease by Development of Tolerance to DNA

Regular administration of cyclophosphamide to NZB/NZW female mice effectively protects against the nephritis that is thought to be a model for human SLE nephritis. Reductions in serologic, histologic, and immunofluorescent parameters of the disease are correlated. Intermittent as well as continuous administration of the drug is effective without the development of leukopenia. Possible mechanisms of drug action and a modified approach to therapy of immune complex disease are discussed.Patients with systemic lupus erythematosus (SLE) develop inflammatory disease of many organs. Best understood is the nephritis that is thought to be From the

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Cyclophosphamide protection in nzb/nzw disease. Mechanisms and therapeutic regimens

Morris

Esterly

Chase

et al. 1976

Arthritis & Rheumatism

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Study of the multiple factors in the pathogenesis of autoimmunity in new zealand mice

Steinberg

Klassen

Raveché

et al. 1978

Arthritis & Rheumatism

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Autoimmune New Zealand mice provide animal models of human systemic lupus erythematosus. Investigations suggest that the disease is multifactorial in origin; genetic, viral, biochemical, and hormonal factors are all capable of modifying the expression of autoimmunity. However, the immune system is the common pathway of disease expression. Early abnormal functioning of the immune system involves excessive effector function and inadequate suppressor function. Since New Zealand mice act as if they are excessively stimulated, the defect in suppressor function may be relative rather than absolute. Thus, excessive B‐cell stimulation cannot be controlled by available regulatory processes. Thymic developmental abnormalities point to an early primary defect in the generation of regulatory T cells. As NZB and NZB/NZW mice pass from neonatal to young adult life, they lose suppressor cell function, probably from the loss of one of at least two cell types that interact to produce suppression. The lost cell appears to be an immature or precursor cell. Anti‐T cell antibodies and immune complexes may accelerate the loss of suppressor cells and thereby lead to more rapid depletion of the suppressor cell precursors. Beneficial therapeutic efforts include administration of suppressor cells or their products, steroid hormones—glucocorticoids and androgens—immunosuppressive drugs, antiinflammatory agents, and antiviral drugs.

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Ribavirin treatment in murine autoimmune disease

Klassen¹,

Williams²,

Reinertsen³

et al. 1979

Arthritis & Rheumatism

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NZB/W F, female mice were treated from 20 weeks of age with ribavirin (a broad spectrum antiviral drug), cyclophosphamide, or saline. Treatment with ribavirin (250 mg/kg twice weekly) prolonged survival from 9.8 to 18.5 months, reduced anti-DNA antibodies, and prevented proteinuria. Ability of ribavirin to prolong survival was dose related when given on a twice weekly schedule. However, daily ribavirin (25 mg/kg/day) was as effective as higher intermittent doses. Optimal ribavirin therapy was equal to cyclophosphamide treatment with regard to prolongation of survival. Ribavirin treatment did not significantly alter the body weight, hematocrit, WBC count, serum immunoglobulins, or Coombs reactivity. No alterations in either cellular or humoral immune responses were noted in NZB/W F, or BALB/c mice treated for prolonged periods with ribavirin. The

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Modification of NZB/NZW F1 Autoimmune Disease by Development of Tolerance to DNA

Cited by 30 publications

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Cyclophosphamide protection in nzb/nzw disease. Mechanisms and therapeutic regimens

Cyclophosphamide protection in nzb/nzw disease. Mechanisms and therapeutic regimens

Study of the multiple factors in the pathogenesis of autoimmunity in new zealand mice

Ribavirin treatment in murine autoimmune disease

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