T cell abnormalities in NZB mice occur independently of autoantibody production. Academic Article uri icon

abstract

  • 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.

published proceedings

  • J Exp Med

author list (cited authors)

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

citation count

  • 74

complete list of authors

  • Taurog, JD||Raveche, ES||Smathers, PA||Glimcher, LH||Huston, DP||Hansen, CT||Steinberg, AD

publication date

  • February 1981