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Study unveils route by which the hormone modulates T cell death

Focus was to assess whether melatonin had a role in regulating the immune response coordinated by helper T lymphocytes

 
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Foto: Divulgação/Wired
Picture shows biochemical pathway by which the hormone melatonin modulates the death of T cells - white blood cells involved in cellular immunity
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Picture shows biochemical pathway by which the hormone melatonin modulates the death of T cells - white blood cells involved in cellular immunity

A study by Brazilian researchers uncovered the biochemical pathway by which melatonin a hormone produced by the pineal gland and immune cells modulate the death-induced activation of certain T cells, which are specialized white blood cells coordinate the immune response against tumors and infectious agents.

The study had the participation of scientists from the Institute of Biomedical Sciences (ICB) and the Faculty of Pharmaceutical Sciences (FCF), University of São Paulo, Institute of Research Immunology / National Institute of Science and Technology (INCT-iii) and the Institute National Cancer (INCA). The findings were published in the Journal of Immunology in an article that merited comment in the same issue.

Author of the article, Gustavo Amarante-Mendes, Professor, Department of Immunology, ICB-USP, said that melatonin is already used clinically to treat sleep disorders, for example. But until now, very little has been explored in relation to the immune system.

The focus of the study was to assess whether melatonin had a role in regulating the immune response coordinated by helper T lymphocytes. This was the scientific question that has united our groups around that work, said the agency FAPESP.

The laboratory led by Amarante-Mendes is dedicated to the study of signaling and cell death in cancer and immune system. One of our lines of research is to study the regulation of the expression of ligands of cell death receptors (death receptors) and signaling performed when these ligands engage their receptors, he said.

The researchers published two papers on the same line of investigation. One, in 2008, in Cell Death and Differentiation, showed regulation of expression of CD95L (FasL) induces death in cells expressing CD95 (Fas) by the lipid mediator prostaglandin E2. In the second paper, demonstrate the same type of regulation by another molecule, melatonin, he said.

Melatonin, he says, is a hormone originally described as being produced in the pineal gland, but increasingly consolidates the concept that it is also produced elsewhere in the body.

Apparently, inflammatory situations in the melatonin production at the site of inflammation is even bigger than the pineal production. Thus, we were interested to study the extent to which this hormone has the effect of modulating the relationship between the immune system and inflammation, he said.

According Amarante-Mendes, the scientific interest in this issue led her group of ICB-USP working in close collaboration with a team led by Ana Campa, FCF-USP coauthor of the article in the Journal of Immunology, who have deep expertise on melatonin .

The first authors of the article, Alziana Moreno da Cunha and Ricardo Pedrosa Weinlich respectively doctoral advisees Ana Campa and Amarante-Mendes, had Grant from FAPESP. Participated in the study Giuliana Patricia Mognol, Bruno Kaufmann and John Paul Robbs Biaso Viola, all of the Inca.

The fundamental question of our project is whether the microenvironment inflammatory / infection produces a soluble factor capable of triggering a signaling pathway that controls the non existence of helper T cells, he said. The helper T cells (also known as T helper or Th), express the CD4 cell surface marker and are the coordinators of the immune response called adaptive. They proliferate after contact with antigen and are able to activate other cell types with effector activity.

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Expansion immune

The group demonstrated in the first article, that in response to molecular patterns present in pathogens, the antigen-presenting cells release prostaglandin E2. "This lipid mediator acts on Th cells, preventing the expression of CD95L, which normally occurs after the antigenic stimulus," he said.

The consequence of these results, the professor from ICB, USP, is that in the absence of CD95L on the surface of Th cells, they suffer the phenomenon known as activation-induced cell death (activation-induced cell death (AICD) - allowing a greater proliferation of these cells.

"Moreover, since CD95L on the surface of Th lymphocytes can also stimulate the death of antigen-presenting cell, blocking this pathway could contribute to the maintenance of the immune response mediated by Th cells," he said.

In the first study, second Amarante-Mendes, the group described a means of recognition of infection, generating a lipid mediator by presenting cells.

"In the second case we show that melatonin produced in the inflammatory response in the presence or absence of infection, it also prevents the increased expression of CD95L. In this particular case, we describe the biochemical pathway completely, showing that melatonin interferes with the activation of NFAT, a transcription factor that is essential for the expression of CD95L, "he said.

In the presence of melatonin, there is activation of NFAT. Therefore, transcription of CD95L does not occur and that allows survival of lymphocytes and expansion of Th immune response.

"Our goal now, both in the case of prostaglandin as in the case of melatonin, is to contextualize these processes in any biological system infection in mice, for example. We are looking to move from basic research on signaling for the understanding of biological relevance of our results" , Amarante-Mendes said.

France

Source: FAPESP
   Palavras-chave:   Melatonin    T lymphocytes    Gustavo Amarante-Mendes    USP    ICB   
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