T cell abnormalities in NZB mice occur independently of autoantibody production

J. D. Taurog, E. S. Raveche, P. A. Smathers, L. H. Glimcher, D. P. Huston, C. T. Hansen, A. D. Steinberg

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


By means of a series of crosses and backcrosses, ZB.CBA/N mice were prepared bearing largely NZB autosomal genes, but having X chromosomes derived only from CBA/N mice. The CBA/N X chromosome carries a gene, xid, that is associated with the lack of a B cell subset necessary for most of the spontaneous autoantibody production by NZB mice. These ZB.CBA/N mice failed to develop autoantibodies to T cells, erythrocytes, or DNA. The availability of mice that were mostly NZB, but which failed to make autoantibodies, especially anti-T cell antibodies, allowed us to study possible T cell regulatory defects in NZB mice in the absence of either antibodies reactive with such T cells or other autoantibodies. We found that such mice had derangements of T cell regulation as did the NZB mice. These observations strongly suggest that the T cell abnormalities of NZB mice are not caused by the B cell hyperactivity of these mice, but rather represent independent defects. Thus, NZB mice appear to have primary defects in both the B cell population and the T cell population. Whether or not these are separate, or derive from a common precursor cell abnormality, remains to be determined.

Original languageEnglish (US)
Pages (from-to)221-234
Number of pages14
JournalJournal of Experimental Medicine
Issue number2
StatePublished - 1981

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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