Published online 16 July 2001. doi:10.1084/jem.194.2.165
© The Rockefeller University Press, 0022-1007/2001/7/165/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 2, July 16, 2001 165-172
Interferon
Stabilizes the T Helper Cell Type 1 Phenotype
Yongkang Zhanga,
Ron Apiladoa,
John Colemana,
Shlomo Ben-Sassonb,c,
Sharon Tsangb,
Jane Hu-Lib,
William E. Paulb, and
Hua Huanga
a The Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153
b The Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
c The Lautenberg Center for General and Tumor Immunology, The Hebrew University School of Medicine, Jerusalem 91120, Israel
Dept. of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, Stritch School of Medicine, Bldg. 102, Rm. 5657, 2160 South First Ave., Maywood, IL 60153.708-216-3913708-216-3349
hhuang{at}lumc.edu
T helper cell (Th)1-primed CD4 T cells from wild-type donors make little interleukin (IL)-4 when restimulated under Th2 conditions. However, such restimulation of Th1-primed cells from interferon (IFN)-
2/– or IFN-
receptor (IFN-
R)–/– mice resulted in substantial production of IL-4 and other Th2 cytokines. Adding IFN-
to the priming culture markedly diminished the capacity of Th1-primed IFN-
2/– cells to express IL-4. Even IFN-
–producing cells from IFN-
R–/– mice could acquire IL-4–producing capacity. Thus, IFN-
is not required for the development of IFN-
–producing capacity, but it plays a critical role in suppressing the IL-4–producing potential of Th1 cells.
Key Words: IL-4 IL-12 differentiation commitment cell cloning
Abbreviations used in this paper: Jak, Janus kinase; RPA, RNase protection assay; SOCS, suppressor of cytokine signaling; STAT, signal transducer and activator of transcription; WT, wild-type.
© 2001 The Rockefeller University Press

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