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Review
. 2015 Apr:37:108-18.
doi: 10.1016/j.yfrne.2014.10.001. Epub 2014 Oct 18.

Neuroendocrine control of photoperiodic changes in immune function

Zachary M Weil  1 , Jeremy C Borniger  2 , Yasmine M Cisse  2 , Bachir A Abi Salloum  2 , Randy J Nelson  2
Affiliations
Review

Neuroendocrine control of photoperiodic changes in immune function

Zachary M Weil et al. Front Neuroendocrinol. 2015 Apr.

Abstract

Seasonal variation in immune function putatively maximizes survival and reproductive success. Day length (photoperiod) is the most potent signal for time of year. Animals typically organize breeding, growth, and behavior to adapt to spatial and temporal niches. Outside the tropics individuals monitor photoperiod to support adaptations favoring survival and reproductive success. Changes in day length allow anticipation of seasonal changes in temperature and food availability that are critical for reproductive success. Immune function is typically bolstered during winter, whereas reproduction and growth are favored during summer. We provide an overview of how photoperiod influences neuronal function and melatonin secretion, how melatonin acts directly and indirectly to govern seasonal changes in immune function, and the manner by which other neuroendocrine effectors such as glucocorticoids, prolactin, thyroid, and sex steroid hormones modulate seasonal variations in immune function. Potential future research avenues include commensal gut microbiota and light pollution influences on photoperiodic responses.

Keywords: Melatonin day length; Neuroendocrine; Photoperiod; Seasonality immune function.

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Figures

Figure
Figure
Photic information is transmitted along the retinohypothalamic tract (RHT) by intrinsically photosensitive retinal ganglion cells (iPRGCs) to the suprachiasmatic nucleus (SCN). Photoperiod is transduced from an environmental cue into a neuroendocrine one via the nighttime secretion of pineal melatonin. Short day lengths are represented physiologically by increased duration of melatonin secretion. Melatonin in turn, regulates immune physiology both directly, through MT1/2 receptors on immune tissues, and indirectly via modulation of several neuroendocrine systems. The combined effect results in a system primed for immediate response to immune threats and stunted long term sickness behavior. RHT, retinohypothalamic tract; SCN: suprachiasmatic nucleus; MT1/2, melatonin receptors 1 and 2; MR, mineralocorticoid receptor; GR, glucocorticoid receptor; DIO3, deiodinase iodothyronine type III; T3, triiodothyronine.
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