Melatonin inhibits fas ligand expression and protects T cells from activation-induced cell death: role of NFAT signaling pathway (2006)
- Authors:
- USP affiliated authors: MENDES, JOAO GUSTAVO PESSINI AMARANTE - ICB ; CAMPA, ANA - FCF
- Unidades: ICB; FCF
- Assunto: IMUNOLOGIA
- Language: Inglês
- Abstract: Introduction and Objectives : Despite the increasing interest in the biological effects of melatonin on the immune system, the effect of this compound on T cells apoptosis remains largely unknown. This is particularly relevant in the context of activationinduced cell death (AICD) because: (i) activated T cells are able to synthesize and to use melatonin; and (ii) at the end of an immune response, apoptosis of effectors T cells is crucial to maintain the homeostasis of the immune system. In this study we investigated the effect of melatonin on AICD and Fas Ligand (FasL) expression, a crucial apoptosis-inducing molecule in AICD. Since NFAT1 plays an important role in FasL gene expression, we further examined the effects of melatonin on its activation. Methods: AICD was induced in a T cell hybridoma (DO11.10) by 18h-stimulation with plate-bound anti-CD3 antibodies. Apoptosis was quantified by cell cycle analysis. FasL expression was measured by RT-PCR, immunostaining and luciferase reporter assays. NFAT activity was assessed by Western blot analysis and fluorescent microscopy. Results : At 1mM, melatonin inhibited DNA fragmentation and the expression of FasL.The effect of melatonin seems to be restricted to the activation phase of the AICD because melatonin did not protect T cells from apoptosis induced by anti-Fas antibodies. As melatonin inhibits the activity of calcineurin, a phosphatase that regulates NFAT1 activation, we analyzed ifthe FasL induction in DO11.10 T cells is regulated by melatonin through a NFAT1-dependent pathway. Indeed, melatonin suppressed the dephosphorylation of NFAT and its translocation to the nucleus, thus blocking expression of FasL and preventing T cell AICD. This inhibition of T cell death induced by melatonin may have important clinical implications, especially in cases in which melatonin is pharmacologically administered. Conclusion: Melatonin inhibits the NFAT1 signaling pathway, thus blocking the Fas ligand expression, preventing anti-CD3-induced T cell death.
- Imprenta:
- Source:
- Título: Abstracts
- Conference titles: Meeting of the Brazilian Society for Immunology
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ABNT
PEDROSA, A M C et al. Melatonin inhibits fas ligand expression and protects T cells from activation-induced cell death: role of NFAT signaling pathway. 2006, Anais.. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo, 2006. . Acesso em: 15 abr. 2026. -
APA
Pedrosa, A. M. C., Weinlich, R., Campa, A., & Amarante-Mendes, J. G. P. (2006). Melatonin inhibits fas ligand expression and protects T cells from activation-induced cell death: role of NFAT signaling pathway. In Abstracts. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Pedrosa AMC, Weinlich R, Campa A, Amarante-Mendes JGP. Melatonin inhibits fas ligand expression and protects T cells from activation-induced cell death: role of NFAT signaling pathway. Abstracts. 2006 ;[citado 2026 abr. 15 ] -
Vancouver
Pedrosa AMC, Weinlich R, Campa A, Amarante-Mendes JGP. Melatonin inhibits fas ligand expression and protects T cells from activation-induced cell death: role of NFAT signaling pathway. Abstracts. 2006 ;[citado 2026 abr. 15 ] - Neutrophils as a specific target for melatonin and kynuramines: effects on cytokine release
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