Study of the multiple factors in the pathogenesis of autoimmunity in New Zealand mice

A. D. Steinberg, L. W. Klassen, E. S. Raveche, N. L. Gerber, J. L. Reinertsen, R. S. Krakauer, D. F. Ranney, M. Eric Gershwin, G. W. Williams, K. Kovacs, J. P. Reeves

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


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 abnormalitis 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.

Original languageEnglish (US)
JournalArthritis and Rheumatism
Issue number5 SUPPL.
StatePublished - 1978
Externally publishedYes

ASJC Scopus subject areas

  • Immunology
  • Rheumatology


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