Abstract
In this issue of the Journal of Biological Rhythms, Zhou et al. (2002) present data from several experiments aimed at identifying effects of photoperiod on the immune systems of two well-established photoperiodic model species: Siberian hamsters (Phodopus sungorus) and Syrian hamsters (Mesocricetus auratus). Their observations are unambiguous: after adaptation to short days, Syrian hamsters exhibited higher numbers of resident auricular lymphocytes, lower rates of spontaneous lymphocyte proliferation, and less interleukin-6 (IL-6) production. Short days had no apparent effect on a contact hypersensitivity (CH) response, on IgM or IgG primary antibody production, or on secondary proliferative responses to an antigen/irritant (dinitrofluorobenzene) in this species. Gonadectomy did not substantially alter the effect of short days on lymphocyte proliferation or on cytokine production. Siberian hamsters likewise exhibited relatively low basal rates of lymphocyte proliferation and IL-6 production in short days. Photoperiod also modified the response to a polyclonal T-cell mitogen in both sensitized and naive individuals, but had no effect on natural killer (NK) cell activity. The data clearly indicate that the immune systems of both Syrian and Siberian hamsters respond to photoperiod. However, based on these observations, the authors conclude that the expression of the immune response is not directly modified or compromised by photoperiod in either of these species. Instead, the authors contend that “photoperiod has no direct effect on immune responses per se in seasonal mammals” (p. 404). The report also reaches a wholly separate conclusion with regard to the role of the hormone leptin in mediating photoperiodic changes in immunity. Our analysis of the data discussed by Zhou et al. and recent work from our laboratory lead us to disagree with these conclusions. Implicit in the authors’ discussion of the data, and
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