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Updated: Apr 26, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
Melatonin as potential inducer of Th17 cell differentiation
1Laboratory of Immunoregulation, Institute of Ecology and Genetics of Microorganisms, Russian Academy of Sciences, Goleva Str. 13, Perm, Russian Federation.
The subset of T lymphocytes producing IL-17 (Th17) plays a key role in the immune system. It has been implicated in host defense, inflammatory diseases, tumorigenesis, autoimmune diseases, and transplant rejection. Careful analysis of the data available holds that Th17 cell subpopulation should be under the direct control of pineal hormone melatonin: the key Th17 differentiation factor RORα serves in the meantime as a high-affinity melatonin receptor. Since the levels of melatonin have diurnal and seasonal variation, as well as substantial deviations in some physiological or pathological conditions, melatonin-dependent regulation of Th17 cells should implicate multiform manifestation, such as influencing the outcome of infectious challenge or determining predisposition, etiology and progression of immune-related morbidities. Another important reason to raise a point of the new melatonin effects is current considering the possibilities of its clinical trials. Especially, the differentiation of Th17 upon melatonin treatment must aggravate the current recession in autoimmune diseases or induce serious complications in pregnancy.
The subset of T lymphocytes producing IL-17 (Th17) plays a key role in the immune system. It has been implicated in host defense, inflammatory diseases, tumorigenesis, autoimmune diseases, and transplant rejection. Careful analysis of the data available holds that Th17 cell subpopulation should be under the direct control of pineal hormone melatonin: the key Th17 differentiation factor RORα serves in the meantime as a high-affinity melatonin receptor. Since the levels of melatonin have diurnal and seasonal variation, as well as substantial deviations in some physiological or pathological conditions, melatonin-dependent regulation of Th17 cells should implicate multiform manifestation, such as influencing the outcome of infectious challenge or determining predisposition, etiology and progression of immune-related morbidities. Another important reason to raise a point of the new melatonin effects is current considering the possibilities of its clinical trials. Especially, the differentiation of Th17 upon melatonin treatment must aggravate the current recession in autoimmune diseases or induce serious complications in pregnancy.
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