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International Immunology, Vol. 6, No. 7, pp. 1081-1090,July 1994
© 1994 Japanese Society for Immunology

Prevention of TCR-mediated apoptosis by the elevation ofcAMP

Sumio Hoshi1,3, Makoto Furutani-Selki1, Masao Seto2, Tomio Tada1 and Yoshihiro Asano1,

1 Department of Immunology, Faculty of Medicine, University of Tokyo Tokyo 113, Japan.
2 Laboratory of Chemotherapy, Aichi Cancer Center Research Institute Nagoya 464, Japan

Correspondence to: Correspondence to: Y. Asano

The stimulation through TCR-CD3 complexes by Immobilized anti-CD3 antibody induced the production of IL-2 and activation-induced cell death (ACD) in the majority of T cell hybridomas. However, some hybridomas produced IL-2 without showing any signs of ACD by the same stimulation, indicating that TCR - CD3-medlated signaling pathways of IL-2 production and of ACD are different. These pathways were discriminated from each other by protein kinase inhibitors and cAMP-elevating reagents such as forskolin. The pathway of IL-2 production but not of ACD was Inhibited by protein Mnase inhibitors. On the other hand, various cAMP-elevating reagents prevented the T cell hybridomas from TCR-mediated ACD with minimal inhibition of IL-2 production. The elevated cytoplasmic cAMP did not block dexamethasone-induced apoptosis. This indicates that apoptosis is regulated by multiple pathways. Furthermore, the inhibitory effect of cAMP is specific for the TCR-mediated signaling pathway of ACD. Messenger RNA for bci-2 was detected after treatment with forskolin.

Keywords: activation-induced cell death, apoptosis, cAMP, bci-2, forskolin

3Present address: Nippon Institute for Biological Science, 2221-1, Shinmachi, Ome, Tokyo 198, Japan

Received 1 November 1993, accepted 11 April 1994.


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