Prevention of TCR-mediated apoptosis by the elevation ofcAMP
Autor: | Makoto Furutani-Selki, Tomio Tada, Yoshihiro Asano, Sumio Hoshi, Masao Seto |
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Rok vydání: | 1994 |
Předmět: |
Programmed cell death
CD3 Complex T-Lymphocytes T cell Molecular Sequence Data Immunology Receptors Antigen T-Cell Apoptosis chemical and pharmacologic phenomena Biology Lymphocyte Activation Dexamethasone Mice chemistry.chemical_compound Aldesleukin Proto-Oncogene Proteins Cyclic AMP medicine Animals Immunology and Allergy RNA Messenger Protein kinase A Hybridomas Forskolin Base Sequence Cell Death Colforsin T-cell receptor General Medicine Protein-Tyrosine Kinases Cell biology medicine.anatomical_structure Proto-Oncogene Proteins c-bcl-2 chemistry Biochemistry Interleukin-2 Signal transduction |
Zdroj: | International Immunology. 6:1081-1090 |
ISSN: | 1460-2377 0953-8178 |
DOI: | 10.1093/intimm/6.7.1081 |
Popis: | 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-mediated 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 kinase 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 bcl-2 was detected after treatment with forskolin. |
Databáze: | OpenAIRE |
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