BMAL1 gene is central in regulating circadian clock and rhythmic gene expression in mammal cells. However, its influence over physiological functions seems to be broader than expected, and it might be involved in unexpected pathways, including immune responses, since people displaying circadian disruptions are more prone to develop chronic inflammatory diseases.
Caroline E. Sutton and colleagues might have found the molecular machinery -or at least one of its important gears- of this mechanism, in this paper published on Nature Communication.
Apparently, BMAL1 plays an important role in the crosstalk between innate and adaptive immunity, since mice that carry myeloid-targeted deletion of this gene display a more severe degree of inflammation, and are way more susceptible to EAE, which seems to be mediated by aberrant secretion of pro-inflammatory citokines by CNS-infiltrating monocytes and increased polarization of pathogenetic T cells.
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