Lymphoproliferative Disorders with Early Lethality in Mice Deficient in Ctla-4
Paul D. Waterhouse, Josef Martin Penninger, Emma M. Timms, Andrew C. Wakeham, Arda Shahinian, Kelvin P. Lee, Craig B. Thompson, Henrik Griesser, Tak W. Mak
Science · 1995 · 2,781 citations
Abstract
The role of the cell-surface molecule CTLA-4 in the regulation of T cell activation has been controversial. Here, lymph nodes and spleens of CTLA-4-deficient mice accumulated T cell blasts with up-regulated activation markers. These blast cells also infiltrated liver, heart, lung, and pancreas tissue, and amounts of serum immunoglobulin were elevated. The mice invariably became moribund by 3 to 4 weeks of age. Although CTLA-4-deficient T cells proliferated spontaneously and strongly when stimulated through the T cell receptor, they were sensitive to cell death induced by cross-linking of the Fas receptor and by gamma irradiation. Thus, CTLA-4 acts as a negative regulator of T cell activation and is vital for the control of lymphocyte homeostasis.
Cite this paper
Waterhouse, P. D., Penninger, J. M., Timms, E. M., Wakeham, A. C., Shahinian, A., Lee, K. P., Thompson, C. B., Griesser, H., & Mak, T. W. (1995). Lymphoproliferative disorders with early lethality in mice deficient in Ctla-4. Science, 270(5238), 985–988. https://doi.org/10.1126/science.270.5238.985
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