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Department of Immunochemistry, German Cancer Research Center (DKFZ), Heidelberg, Germany
Exposure of T cells to the macrophage products hydrogen peroxide
(HP) or L-lactate (LAC) was previously shown to enhance
IL-2 production and to modulate glutathione (GSH) status. We now found
that 50 µM HP and 30 mM LAC enhanced strongly the transcription from
the IL-2 promoter in Jurkat T cells after stimulation with
anti-CD28 together with or without anti-CD3 but not with
anti-CD3 Abs alone. Therefore, we used anti-CD3 plus
anti-CD28-stimulated cells to investigate the effect of the GSH
reductase inhibitor 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) on the
signal cascade. BCNU enhanced the transcription to a similar extent as
HP or LAC. Lowering the intracellular GSH/GSH disulfide ratio by BCNU,
HP, or NO resulted in all cases in the fulminant enhancement of
Jun-N-terminal kinase and p38 mitogen-activated protein kinase but not
extracellular signal-regulated kinase 1/2. Jun-N-terminal kinase and
NF-
B activation was enhanced through pathways involving Rac, Vav1,
PKC
, p56lck, p59fyn, and IB kinases. In a
cell-free system, the autophosphorylation of rFyn was stimulated by GSH
disulfide but not by HP. These findings suggest that the oxidation of
the cellular thiol pool may play a role as an amplifying mechanism for
TCR/CD3 signals in immune responses.
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