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Melatonin reduces inflammatory response in peripheral T helper lymphocytes from relapsing‐remitting multiple sclerosis patients
Author(s) -
ÁlvarezSánchez Nuria,
CruzChamorro Ivan,
DíazSánchez María,
SarmientoSoto Helia,
MedranoCampillo Pablo,
MartínezLópez Alicia,
Lardone Patricia J.,
Guerrero Juan M.,
CarrilloVico Antonio
Publication year - 2017
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/jpi.12442
Subject(s) - melatonin , multiple sclerosis , immune system , immunology , peripheral blood mononuclear cell , cytokine , medicine , effector , melatonin receptor , endocrinology , biology , in vitro , biochemistry
Multiple sclerosis ( MS ) is a neuroinflammatory disease of the central nervous system in which the immune system plays a central role. In particular, effector populations such as T helper (Th) 1, Th9, Th17, and Th22 cells are involved in disease development, whereas T regulatory cells (Tregs) are associated with the resolution of the disease. Melatonin levels are impaired in patients with MS , and exogenous melatonin ameliorates the disease in MS animal models by modulating the Th1/Th17/Treg responses and also improves quality of life and several symptoms in patients with MS . However, no study has examined melatonin's effect on T cells from relapsing‐remitting MS ( RR ‐ MS ) patients. Therefore, the objectives of the present study were to evaluate the effects of the in vitro administration of melatonin to peripheral blood mononuclear cells ( PBMC s) from 64 RR ‐ MS patients and 64 sex‐ and age‐matched healthy subjects on Th1, Th9, Th17, Th22, and Treg responses and to analyze the expression of the melatonin effector/receptor system in these cells. Melatonin decreased Th1 and Th22 responses in patients, whereas it did not affect the Th17 and Treg subsets. Melatonin also promoted skewing toward a more protective cytokine microenvironment, as shown by an increased anti‐inflammatory/Th1 ratio. Furthermore, for the first time, we describe the overexpression of the melatonin effector/receptor system in PBMC s from patients with MS ; this alteration might be relevant to the disease because acetylserotonin O‐methyltransferase expression significantly correlates with disease progression and T effector/regulatory responses in patients. Therefore, our data suggest that melatonin may be an effective treatment for MS .

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