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,
*
Department of Pathology,
Committee on Immunology, and
Department of Medicine, University of Chicago, Chicago, IL 60637; and
Department of Surgery, University of Wisconsin, Madison, WI 53792
Studies in Jurkat cells have shown that combined stimulation
through the TCR and CD28 is required for activation of c-Jun N-terminal
kinase (JNK), suggesting that JNK activity may mediate the
costimulatory function of CD28. To examine the role of JNK signaling in
CD28 costimulation in normal T cells, murine T cell clones and
CD28+/+ or CD28-/- TCR transgenic T cells
were used. Although ligation with anti-CD28 mAb augmented JNK
activation in Th1 and Th2 clones stimulated with low concentrations of
anti-CD3 mAb, higher concentrations of anti-CD3 mAb alone were
sufficient for JNK activation even in the absence of anti-CD28. JNK
activity was comparably induced in both CD28+/+ and
CD28-/- 2C/recombinase-activating gene
2(RAG2)-/- T cells stimulated with anti-CD3 mAb
alone, and with Ld/peptide dimers, a direct 
TCR
ligand. Moreover, JNK activation was also detected in
2C/RAG2-/- T cells stimulated with P815 cells that
express the relevant alloantigen Ld whether or not B7-1 was
coexpressed. However, IL-2 production by both Th1 clones and
CD28+/+ 2C/RAG2-/- T cells was detected only
upon TCR and CD28 coengagement. Thus, CD28 coligation is not necessary,
and stimulation through the TCR is sufficient, for JNK activation in
normal murine T cells. The concept that JNK mediates the costimulatory
function of CD28 needs to be reconsidered.
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