The neuroimmunology of social-stress-induced sensitization
Open accessAbstract
Myriad clinical findings provide links between chronic stressors, inflammation, and mood disorders. Furthermore, traumatic or chronic exposure to psychological stressors may promote stress sensitization, in which individuals have long-term complications, including increased vulnerability to subsequent stressors. Post-traumatic stress disorder (PTSD) is a clinically relevant example of stress sensitization. PTSD alters neuronal circuitry and mood; however, the mechanisms underlying long-term stress sensitization within this disorder are unclear. Rodent models of chronic social defeat recapitulate several key physiological, immunological, and behavioral responses associated with psychological stress in humans. Repeated social defeat (RSD) uniquely promotes the convergence of neuronal, central inflammatory (microglial), and peripheral immune (monocyte) pathways, leading to prolonged anxiety, social withdrawal, and cognitive impairment. Moreover, RSD promotes stress sensitization, in which mice are highly sensitive to subthreshold stress exposure and recurrence of anxiety weeks after the cessation of stress. Therefore, the purpose of this Review is to discuss the influence of social-defeat stress on the immune system that may underlie stress sensitization within three key cellular compartments: neurons, microglia, and monocytes. Delineating the mechanisms of stress sensitization is critical in understanding and treating conditions such as PTSD.
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The CSDS model effectively induces behavioral phenotypes similar to human anxiety and depression, with high modeling success rates and prolonged social avoidance.
“The CSDS model stands out due to its direct simulation of social conflict through “resident–intruder” interactions, effectively inducing behavioral phenotypes similar to human anxiety and depression, with high modeling success rates and prolonged social avoidance, making it a classic paradigm for studying stress-related mental disorders [5,17].”
From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [17]
The Social defeat stress section says social defeat in mice produces anxiety-like behavior and social avoidance that parallel aspects of human mood disorders. It describes chronic social defeat as a classic protocol, but does not establish a high success rate or prolonged social avoidance for that protocol; its statement that resilience is rare concerns the related, more intense RSD model. The Social defeat and sensitization section reports increased avoidance 24 days later after an additional stressor, not continuous avoidance following CSDS alone. Page numbers are unavailable in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAdrenalectomy-model mice fail to exhibit the typical stress-induced immune cell mobilization response, characterized by lymphocyte suppression and myeloid cell expansion.
“These results suggest that adrenalectomy-model mice fail to exhibit the typical stress-induced immune cell mobilization response, which is characterized by lymphocyte suppression and myeloid cell expansion [3,17,42].”
From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [17]
The Social defeat stress section reports that repeated social defeat increases production of monocytes and neutrophils and releases inflammatory monocytes into circulation, supporting the myeloid-cell expansion part of the cited background claim. The passages found do not describe lymphocyte suppression. The statement about adrenalectomy-model mice is framed as the citing authors’ own interpretation, not a finding attributed to this source. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe acute social defeat stress response supports the fight-or-flight reaction by fulfilling energy demands and modulating immune responses.
“This response supports the “fight-or-flight” reaction by fulfilling energy demands and modulating immune responses”
From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [17]
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- F]-FEPPA PET imaging. Brain Behav. Immun. Health 16, 100287 (2021). [PubMed: 34589784]
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“…of social conflict through “resident–intruder” interactions, effectively inducing behavioral phenotypes similar to human anxiety and depression, with high modeling success rates and prolonged social avoidance, making it a classic paradigm for studying stress-related mental disorders [5,17].”
- Authors
- Biltz, R. G., Sawicki, C. M., Sheridan, J. F., & Godbout, J. P.
- Affiliations
- The Ohio State University Wexner Medical Center (US)
- The Ohio State University (US)
- Corresponding author
- Sheridan, John F.
- Godbout, Jonathan P.
- Venue
- Nature Immunology
- Published
- 2022-11
- Volume
- 23
- Issue
- 11
- Pages
- 1527-1535
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC10000282
- OpenAlex
- W4308918565
- Cited by
- 132
- References
- 99
- Citations by year
- 2026: 29 · 2025: 49 · 2024: 40 · 2023: 13 · 2022: 1
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (119670, 116670)
- U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (DE014320, DE026075)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- stress sensitization, chronic social defeat, repeated social defeat, post-traumatic stress disorder, neuroimmunology, microglia, monocytes, neuroinflammation, peripheral immune response, anxiety, social withdrawal, cognitive impairment, mood disorders, chronic stress
- MeSH terms
- Animals, Anxiety, Humans, Monocytes, Stress, Psychological, Neuroimmunomodulation, Microglia, Mice
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