Multiple neuroendocrine pathways mediate seasonal immunity.

Regulating the activity of the immune system involves a balancing act that must allow organisms to recognize and resist pathogens while at the same time keeping in check the potentially harmful effects of an overactive immune system. Activation of the immune system can be energetically costly (3,4) and the energy allocated to immune activity at any given time likely represents a trade-off between physiological functions relating to growth and reproduction versus survival. In support of this hypothesis, activating the immune system of Siberian hamsters by simulated infection in the laboratory results in inhibition of reproductive maturation (14). At temperate latitudes, winter poses a seasonally recurring energetic bottle-neck, when temperatures are relatively low and food availability is decreased, necessitating a trade-off between reproduction and immune function. For more than a decade, Nelson and colleagues have characterized the seasonal regulation of immune function in rodents (7,8,9). In common with the seasonal quiescence and reactivation of the reproductive system, seasonal alterations in the function of the immune system are cued by changes in day length (7,8). Both reproductive and immunological seasonality in this species are dependent on photoperiod-driven changes in melatonin production (17). In Siberian hamsters, exposure to short photoperiods in the laboratory induces regression of the gonads and withdrawal of gonadal steroid production. In parallel with reproductive quiescence, short days also alter the immune system. Increases in the number of circulating leukocytes (e.g., T-cells, Page 1 of 7 Articles in PresS. Am J Physiol Regul Integr Comp Physiol (December 5, 2007). doi:10.1152/ajpregu.00856.2007