© The Rockefeller University Press, 0022-1007/1997/6/1897/ $5.00
The Journal of Experimental Medicine, 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
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 I
B
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 TCRhi 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.
Address correspondence to Mark Boothby or Dean Ballard, Department of Microbiology and Immunology, Vanderbilt University Medical School, Nashville, Tennessee 37232-2363.
The authors acknowledge A. Cherrington and W. Armistead for technical assistance; J. Wright and C. Pettipher (Vanderbilt Cancer Center Transgenic Core) for DNA microinjections; A. Lackey (Cytometry Associates, Brentwood, TN) and J. Price (Vanderbilt Cancer Center Core) for expert flow cytometry analyses; L. Glimcher, E. Oltz, T. Aune, G. Miller, D. Perkins, T. Laufer, J. Chen, L. Van Kaer, E. Robey, D. Kioussis, L. Kelley, and P. Fink for helpful discussions; and E. Vance for help with manuscript preparation. D.W. Ballard is an investigator of the Howard Hughes Medical Institute (HHMI). Supported by National Institutes of Health grant AI-33839 and the Howard Hughes Medical Institute (D.C. Scherer, J.A. Brockman, D.W. Ballard), and by National Institutes of Health grant AI-36997, GM-42550, and the Leukemia Society of America (A.L. Mora, M.R. Boothby).
1Abbreviations used in this paper: BrdU, 5-bromo-2'-deoxyuridine;
B-pd,
B enhancer sequences based on the IL-2R
promoter; NF-
B, nuclear factor-
B; SP, single positive.

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