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Published online before print December 5, 2005

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(Journal of Leukocyte Biology. 2006;79:369-377.)
© 2006 by Society for Leukocyte Biology

Fas costimulation of naïve CD4 T cells is controlled by NF-B signaling and caspase activity

Mikael Maksimow^*,, Thomas S. Söderström^,,, Sirpa Jalkanen^*, John E. Eriksson^,¶ and Arno Hänninen^*,1

^* MediCity Research Laboratory and Department of Medical Microbiology, University of Turku, and National Public Health Institute, Turku, Finland;
Turku Centre for Biotechnology, University of Turku, and Åbo Akademi University, Finland;
Department of Biology, Åbo Akademi University, Turku, Finland;
^¶ Department of Biology, Laboratory of Animal Physiology, University of Turku, Finland; and
Turku Graduate School of Biomedical Sciences, Finland

¹Correspondence: MediCity Research Laboratory, University of Turku, Tykistökatu 6A, 20520 Turku, Finland. E-mail: arno.hanninen{at}utu.fi

Fas ligation induces apoptosis of activated T cells via the caspase cascade but can also mediate costimulatory signals to naïve T cells at the time of activation. We have previously shown that Fas ligation of naïve CD4 T cells activated by dendritic cells induces death or accelerates their proliferation and increases interferon- (IFN-) production. To understand this costimulation, we investigated the roles of caspases and nuclear factor (NF)-B in survival and proliferation of responding T cells. Fas ligation increased caspase-3 and -8 activities during T cell activation, irrespective of cell fate. The accelerated proliferation induced by Fas ligation could be reduced by selective inhibition of both caspases. Inhibition of NF-B simultaneously with Fas ligation inhibited the increased IFN- production and caused uniform death of all responding T cells. Thus, Fas-mediated costimulation of naïve CD4 T cells is driven by active caspases, and NF-B acts as a dominant survival-supporting factor of Fas-costimulated cells containing high levels of activated caspase-8 and -3.

Key Words: T cell activation • lymphocyte • apoptosis • dendritic cell • cell proliferation

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