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Tanja Lange, MD; Stoyan Dimitrov, MSc; Horst-Lorenz Fehm, MD; Jürgen Westermann, MD; Jan Born, PhD

Arch Intern Med. 2006;166:1695-1700.

Background  Sleep is considered to strengthen immune defense. We hypothesized that sleep achieves this effect by shifting the balance between types 1 and 2 cytokine activity toward increased type 1 activity, thereby supporting adaptive cellular immune responses.

Methods  We analyzed monocyte-derived type 1 (interleukin 12 [IL-12]) and type 2 (IL-10) cytokines by means of multiparametric flow cytometry in healthy human subjects (n = 11) during a regular sleep-wake cycle and 24 hours of wakefulness.

Results  Sleep increased the number of IL-12–producing monocytes and concurrently decreased the number of IL-10–producing monocytes, thereby inducing clear rhythms in these cells, with maximum numbers at 2:20 and 11:30 AM, respectively. The rhythms were completely absent during continuous wakefulness. Correlation analyses and supplementary in vitro studies suggest that high prolactin and low cortisol levels are factors contributing to the shift in the IL-12/IL-10 ratio toward increased IL-12 activity during sleep.

Conclusions  Monocyte-derived IL-12 and IL-10 play a critical role for tuning the synapse between antigen-presenting cells and lymphocytes. By preferentially supporting type 1 IL-12 activity, sleep induces a 24-hour oscillation between predominant types 1 and 2 cytokines and, in this way, acts to globally increase the efficacy of adaptive immune responses. Improving sleep could represent a therapeutic option to enhance the success of vaccinations and success in the treatment of diseases (eg, atopic dermatitis and human immunodeficiency virus infection) that are characterized by type 2 cytokine overactivity.

Author Affiliations: Departments of Internal Medicine (Drs Lange and Fehm), Neuroendocrinology (Mr Dimitrov and Dr Born), and Anatomy (Dr Westermann), University of Lübeck, Lübeck, Germany.

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