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Original Article |
Stabilizes the T Helper Cell Type 1 Phenotype
Correspondence to: Hua Huang, 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. Tel:708-216-3349 Fax:708-216-3913 E-mail: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-4producing capacity. Thus, IFN-
is not required for the development of IFN-
producing capacity, but it plays a critical role in suppressing the IL-4producing potential of Th1 cells.
Key Words: IL-4, IL-12, differentiation, commitment, cell cloning
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