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,§
*
Division of Immunobiology, Research Institute for Biological Sciences, Science University of Tokyo, Noda City, Chiba, Japan;
Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan;
Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan;
§
CREST, Japan Science and Technology Corporation, Tokyo, Japan; and
¶
Cadus Pharmaceutical Corp., Tarrytown, NY 10591
The development of Th1 and Th2 cells is determined by the type of
antigenic stimulation involved in the initial cell activation step.
Evidence indicates that costimulatory signals, such as those delivered
by CD28, play an important role in Th2 development, but little is known
about how CD28 costimulation contributes to Th2 development. In this
study, TCR cross-linking was insufficient for Th2 development, while
the addition of CD28 costimulation drastically increased Th2 generation
through the IL-4-mediated pathway. Th2 generation following CD28
costimulation was not simply explained by the enhancement of IL-4
production in naive T cells. To generate Th2 cells after TCR
cross-linking only, it was necessary to add a 20- to 200-fold excess of
IL-4 generated after TCR and CD28 stimulation. TCR cross-linking
increased the expression level and binding property of the IL-4R, but
enhanced the sensitivity to IL-4 only slightly. In contrast, as
evidenced by the enhanced phosphorylation of Jak3, the IL-4R
-chain,
and STAT6 following IL-4 stimulation, CD28 costimulation increased
IL-4R sensitivity without affecting its expression and binding
property. This evidence of the enhancement of IL-4R sensitivity
increases our understanding of how CD28 costimulation accelerates Th2
development.
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