How does insufficient sleep impact immune function and infection susceptibility?
Executive summary
Insufficient sleep alters immune-cell profiles, raises inflammatory markers, and reduces vaccine and infection defenses: studies report one night (24 h) of sleep loss changes monocyte and other immune-cell distributions to patterns seen in obesity (linked to chronic inflammation) [1] [2]. Chronic or repeated short sleep is associated with low‑grade systemic inflammation, impaired T‑cell and antibody responses, and greater susceptibility to infections in animal and human studies [3] [4].
1. Sleep loss reshuffles immune cells — immediate effects
Acute sleep deprivation produces rapid changes in circulating immune cells and inflammatory signals. Laboratory work in humans shows severe or 24‑hour sleep loss “jolts” the immune system and changes white‑blood‑cell counts; a 2025 Journal of Immunology study found a single 24‑hour period altered monocyte subsets in healthy volunteers to resemble those seen in obesity-related inflammation [5] [1] [2]. Frontiers and other reviews summarize that acute loss can raise pro‑inflammatory cytokines and shift NK, B‑cell and T‑cell proportions within hours to days [6] [3].
2. Chronic short sleep causes persistent inflammatory tone
Multiple reviews link ongoing sleep restriction to a chronic low‑grade inflammatory state. Chronic sleep deprivation is described as an “unspecific state of chronic stress” that perpetuates systemic inflammation, which epidemiological and experimental work ties to metabolic and neurodegenerative risk [3] [7] [4]. Narrative and integrative reviews emphasize that repeated insufficient sleep maintains higher baseline inflammatory mediators versus normal sleepers [8] [9].
3. Impaired host defense: vaccines and infections
Sleep loss reduces effective immune defenses. Human studies show reduced antibody responses to vaccination after sleep restriction and increased incidence of common colds with poor sleep efficiency [3]. Animal models provide stronger causal signals: sleep‑deprived mice and rats experienced higher mortality after septic challenge and systemic invasion by opportunists, demonstrating that an activated but dysregulated immune state does not reliably protect against pathogens [4] [10].
4. Mechanisms discussed in the literature
Authors propose multiple, interacting mechanisms: altered cytokine rhythms, disrupted circadian genes in brain and immune tissues, shifts in sympathetic/cortisol signaling, melatonin reduction, and gut‑microbiota‑immune axes [10] [3] [9]. Transcriptomic meta‑analyses in sleep‑deprived mice show downregulation of immune‑related genes and circadian disruption, while reviews point to cortisol and autonomic changes as mediators of immune dysregulation [10] [7].
5. How robust is the evidence — strengths and limits
Evidence spans controlled human lab studies, observational cohorts, animal experiments and molecular reviews, giving convergent signals that sleep affects immunity [4] [3] [6]. Limitations noted in the sources: single‑night effects can vary by timing of blood draws and circadian phase; many mechanistic claims rely on animal models; and small sample sizes in some human studies mean effect sizes and generalisability need further work [3] [1] [11]. Reviews explicitly caution that one night’s changes do not always equal clinically meaningful risk in every person [3].
6. Competing viewpoints and unanswered questions
Most sources agree sleep loss perturbs immune function, but they differ on magnitude and clinical translation. Some studies emphasize transient immune activation after one night (acute stress‑like response), while chronic studies report net immunosuppression and poorer vaccine responses [5] [3]. Sources call for more work to trace which immune changes predict real‑world infection risk, how reversible changes are, and the precise roles of melatonin and microbiome pathways [10] [9].
7. Practical implications — what the reporting supports
The assembled literature supports treating regular adequate sleep as part of infection prevention and vaccine planning: habitual short sleepers show diminished vaccine antibody responses and higher illness risk in studies, and acute total sleep loss produces measurable pro‑inflammatory shifts [3] [1] [2]. Reviews and narrative articles recommend addressing chronic sleep restriction to reduce low‑grade inflammation linked to long‑term disease risk [7] [8].
8. Transparency: caveats about current reporting
Available sources do not provide population‑level estimates of how much increased infection risk follows specific amounts of lost sleep (not found in current reporting). Several mechanistic claims rely on animal models and small human cohorts; authors themselves flag these limitations and call for larger, longer human trials to quantify clinical impact [4] [3] [11].
Summary: Multiple lines of evidence show insufficient sleep perturbs immune cell distributions, raises inflammatory signaling, impairs vaccine responses and—especially when chronic—weakens host defense in ways that increase susceptibility to infections. Reviews and new 2025 studies converge on this conclusion while also acknowledging gaps in translating short‑term laboratory changes into precise population risks [1] [3] [4].