Melatonin and its oxidation product AFMK inhibit FasL expression and protects T cells from activation-induced cell death (2005)
- 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 activation-induced cell death (AICD) because: activated T cells are able to synthesize and to use melatonin; and at the end of an immune response, apoptosis of effector T cells are crucial to maintain the homeostasis of the immune system and to avoid, among other things, autoimmune reactions. In this study we investigated the effect of melatonin and its oxidation product AFMK on AICD. Methods: Apoptosis and FasL expression were measured in T cell hybridoma (DO11.10) by flow cytometry and RT-PCR, respectively, after stimulation with anti-CD3 antibodies. Results: At 1mM, melatonin and AFMK inhibited approximately 70% of DNA fragmentation and the expression of FasL. The effect of melatonin and AFMK seems to be restricted to the activation phase of the AICD because neither melatonin nor AFMK protected T cells from apoptosis induced by anti-Fas antibodies. The antioxidant activities of melatonin and AFMK have been considered as the operative mechanism for most of the biological effects triggered by melatonin. In comparison with the antioxidant N-acetyl-cisteine, melatonin and AFMK were more effective in inhibiting T cells death and FasL expression, thus suggesting that the action of melatonin and AFMK includeadditional activities beyond their antioxidant property. The inhibition of T cell death induced by melatonin and AFMK may have important clinical implications, especially in cases in which melatonin is pharmacologically administered. Conclusion: Melatonin and AFMK prevented anti-CD3-induced T cell death by blocking the FasL expression
- Imprenta:
- Publisher: Comissão de Cultura e Extensão Universitária do ICB/USP
- Publisher place: São Paulo
- Date published: 2005
- Source:
- Título do periódico: Resumos
- Conference titles: Congresso do Instituto de Ciências Biomédicas
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ABNT
PEDROSA, Alziana Moreno da Cunha et al. Melatonin and its oxidation product AFMK inhibit FasL expression and protects T cells from activation-induced cell death. 2005, Anais.. São Paulo: Comissão de Cultura e Extensão Universitária do ICB/USP, 2005. . Acesso em: 16 abr. 2024. -
APA
Pedrosa, A. M. da C., Weinlich, R., Campa, A., & Amarante-Mendes, J. G. P. (2005). Melatonin and its oxidation product AFMK inhibit FasL expression and protects T cells from activation-induced cell death. In Resumos. São Paulo: Comissão de Cultura e Extensão Universitária do ICB/USP. -
NLM
Pedrosa AM da C, Weinlich R, Campa A, Amarante-Mendes JGP. Melatonin and its oxidation product AFMK inhibit FasL expression and protects T cells from activation-induced cell death. Resumos. 2005 ;[citado 2024 abr. 16 ] -
Vancouver
Pedrosa AM da C, Weinlich R, Campa A, Amarante-Mendes JGP. Melatonin and its oxidation product AFMK inhibit FasL expression and protects T cells from activation-induced cell death. Resumos. 2005 ;[citado 2024 abr. 16 ] - 'N POT.1'-acetyl-'N POT.2'-formyl-5-methoxykynuramine: a metabolite of melatonin with strong biological activities
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- Neutrophils as a specific target for melatonin and kynuramines: effects on cytokine release
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