The Journal of Experimental Medicine
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Published 18 January 2005. doi:10.1084/jem.20041538
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 2, 181-187
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BRIEF DEFINITIVE REPORT

 NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

Tobias Bopp1, Alois Palmetshofer3, Edgar Serfling3, Valeska Heib1, Steffen Schmitt2, Christoph Richter1, Matthias Klein1, Hansjörg Schild1, Edgar Schmitt1, and Michael Stassen1

1 Institute of Immunology, Johannes Gutenberg University, 55131 Mainz, Germany
2 Center for Natural Sciences and Medicine, Johannes Gutenberg University, 55131 Mainz, Germany
3 Institute of Pathology, Department of Molecular Pathology, University of Würzburg, 97080 Würzburg, Germany

CORRESPONDENCE Michael Stassen: stassenm{at}uni-mainz.de

The phenotype of NFATc2–/– c3–/– (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4+ CD25+ T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family–related gene (GITR) and CD25. However, neither wild-type nor DKO CD4+ CD25+ regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4+ CD25– T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4+ CD25+ T reg cells but renders conventional CD4+ T cells unresponsive to suppression, underlining the importance of NFAT proteins for sustaining T cell homeostasis.

E. Schmitt and M. Stassen share senior authorship for this work.


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