J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/06/1897/11 $2.00
Volume 185, Number 11, June 2, 1997 1897-1907

Perturbation of the T Lymphocyte Lineage In Transgenic Mice Expressing a Constitutive Repressor of Nuclear Factor (NF)-B

By Mark R. Boothby,^* Ana L. Mora,^* David C. Scherer,^*§ Jeffrey A. Brockman,^*§ and Dean W. Ballard^*§

From the ^* Department of Microbiology and Immunology;  Rheumatology Division, Department of Medicine; and the ^§ Howard Hughes Medical Institute, Vanderbilt University Medical Center, Nashville, Tennessee 37232

Members of the nuclear factor (NF)-B/Rel family transcription factors are induced during thymic selection and in mature T lymphocytes after ligation of the T cell antigen receptor (TCR). Despite these findings, disruption of individual NF-B/Rel genes has revealed no intrinsic defect in the development of mature T cells, perhaps reflecting functional redundancy. To circumvent this possibility, the T cell lineage was targeted to express a trans-dominant form of IB that constitutively represses the activity of multiple NF-B/Rel proteins. Transgenic cells expressing this inhibitor exhibit a significant proliferative defect, which is not reversed by the addition of exogenous interleukin-2. Moreover, mitogenic stimulation of splenocytes leads to increased apoptosis of transgenic T cells as compared with controls. In addition to deregulated T cell growth and survival, transgene expression impairs the development of normal T cell populations as evidenced by diminished numbers of TCR^hi CD8 single-positive thymocytes. This defect was significantly amplified in the periphery and was accompanied by a decrease in CD4⁺ T cells. Taken together, these in vivo findings indicate that the NF-B/Rel signaling pathway contains compensatory components that are essential for the establishment of normal T cell subsets.

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