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Cited by 115Cytokine Signaling Pathways and InteractionsSleep and Wakefulness ResearchCircadian rhythm and melatonin

Sleep enhances IL‐6 trans‐signaling in humans

Dimitrov, Stoyan, Lange, Tanja, Benedict, Christian, Nowell, Mari A., Jones, Simon A., Scheller, Jürgen, Rose‐John, Stefan, Born, Jan +8 more·2006·The FASEB Journal
DOI 10.1096/fj.06-5754fje
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Abstract

Sleep is commonly considered to support immune defense. The underlying sleep‐immune interaction appears to rely critically on cytokines, like interleukin‐6 (IL‐6), that combine effects on immune and neuronal functions. The IL‐6 signal is conveyed in two ways: it stimulates a restricted group of (mostly immune) cells via membrane‐bound IL‐6 receptors (mIL‐6R) by forming a complex with soluble IL‐6R (sIL‐6R), and it stimulates (via membrane‐bound gp130) a great variety of other cell types—a process termed trans ‐signaling. Focusing on the receptor side of IL‐6 signaling, we examined the effect of sleep on sIL‐6R plasma concentrations, mIL‐6R expression, plasma sgp130, and numbers of IL‐6‐producing monocytes in healthy humans who were tested during a regular sleep‐wake cycle and 24 h of wakefulness while blood was sampled repeatedly. Sleep strongly enhanced concentrations of sIL‐6R, exceeding wake levels by 70% at the end of sleep. This rise was due to an increase in the PC (proteolytic cleavage) rather than the DS (differentially spliced) variant of sIL‐6R. Sleep did not affect IL‐6‐producing monocytes, mIL‐6R density, or sgp130 concentrations. The selective increase in sIL‐6R implicates an enhanced trans ‐signaling capacity whereby sleep distinctly widens the profile of IL‐6 actions, enabling an integrated influence on brain and peripheral organs.—Dimitrov, S., Lange, T., Benedict, C., Nowell, M. A., Jones, S. A., Scheller, J., Rose‐John, S., Born, J. Sleep enhances IL‐6 trans‐signaling in humans. FASEB J. 20, E1599 –E1609 (2006)

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Crossref · 10.1096/fj.06-5754fje

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61 of 61 references verified0 citation errors · 0 not checkable

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  • Even when sleep-deprived, monocytes show an IL-6 production peak at 0200 hours.

    “Dimitrov et al (2006) have found that monocyte production of IL-6 also peaks at 0200 hours even in the midst of sleep deprivation.”

    From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Dimitrov et al, 2006

  • At night, IL-6 rises together with a marked increase in circulating IL-6R.

    “Along with nocturnal increase in IL-6, there is a robust increase in circulating levels of IL-6R (Dimitrov and Lange et al, 2006).”

    From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Dimitrov and Lange et al, 2006

  • Total monocyte counts, lymphocyte counts, and major lymphocyte subsets (B cells, CD4 and CD8 T cells, NK cells) have been found either reduced by sleep or unchanged compared with acute or prolonged sleep reduction in humans.

    “Similarly, total monocyte counts, lymphocyte counts, and the major lymphocyte subsets (i.e., B cells, CD4 and CD8 T cells, NK cells), have been found to be either reduced by sleep (46, 67, 148, 251, 254, 480, 556, 580) or unchanged (3, 69, 103, 122, 152, 178, 224, 234, 263, 338, 418, 463, 469) when compared with acute or prolonged sleep reduction in humans.”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [148]

  • Sleep might support the migration of lymphocytes, thus supporting the formation of immunological memory.

    “sleep might rather support the migration of lymphocytes, thus supporting the formation of immunological memory.”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [148]

  • Sleep reduces the number of APCs and T cells in the blood, probably by redistributing these cells to lymph nodes.

    “Sleep reduces the number of APCs and T cells in the blood, probably by redistributing these cells to lymph nodes (67, 143, 148, 169)”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [148]

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Authors
Dimitrov, S., Lange, T., Benedict, C., Nowell, M. A., Jones, S. A., Scheller, J., Rose‐John, S., Born, J., Dimitrov, S., Lange, T., Benedict, C., Nowell, M. A., Jones, S. A., Scheller, J., Rose‐John, S., & Born, J.
Venue
The FASEB Journal
Publisher
Wiley
Published
2006-08-15
Volume
20
Issue
12
Pages
2174-2176
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
DOI
10.1096/fj.06-5754fje
OpenAlex
W2089623849
Semantic Scholar
f57ab1a45668acdae5874b167770f0412c77ec30
Cited by
115
References
61
Citations by year
2026: 3 · 2025: 4 · 2024: 10 · 2023: 2 · 2022: 11 · 2021: 8 · 2020: 3 · 2019: 8 · 2018: 4 · 2017: 6 · 2016: 5 · 2015: 9 · 2014: 7 · 2013: 6 · 2012: 6
FWCI
2.43
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The FASEB Journal (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Keywords
sleep, interleukin-6, IL-6 trans-signaling, soluble IL-6 receptor, soluble gp130, sleep-wake cycle, cytokine signaling, sleep-immune interaction
MeSH terms
Adult, Humans, Male, Monocytes, Sleep, Solubility, Tissue Distribution, Signal Transduction, Interleukin-6, Cytokines, Receptors, Interleukin-6

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