Genetic and molecular genetic studies of murine and human lupus.

A. D. Steinberg, D. M. Klinman, D. L. Kastner, M. F. Seldin, W. C. Gause, C. L. Scribner, J. L. Britten, J. N. Siegel, J. D. Mountz

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Mice and humans with systemic lupus erythematosus (SLE) have been studied with regard to cellular, genetic and molecular genetic abnormalities. B cell hyperactivity and autoantibody production are the hallmarks of this illness. In humans with SLE, there is increased stem cell, B cell precursor and B cell proliferation. The same is true of NZB mice. In lpr/lpr and gld/gld mice, marked expansion of a subpopulation of T cells allows extrathymic terminal T cell maturation and secondary B cell hyperactivity. Androgens suppress these processes and polyclonal immune activators accelerate them. Three types of genes are identified: inducing genes, accelerating genes and background genes. These give rise to abnormal expression of various cellular oncogenes, T cell receptor genes and immunoglobulin genes. The data suggest that abnormal immune regulation plays a critical role in the development of SLE, with polyclonal B cell activation being common to both mice and humans with SLE. Different genetic and cellular abnormalities underlie the ultimate syndrome, the common denominator, generalized autoimmunity, that we call SLE.

Original languageEnglish (US)
Pages (from-to)166-176
Number of pages11
JournalJournal of Rheumatology
Volume14 Suppl 13
StatePublished - Jun 1987
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Rheumatology
  • Immunology and Allergy
  • Immunology


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