ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Oxytocin-Mediate Modulation of Splenic Immunosuppression in Chronic Social Stress Through Neuroendocrine Pathways.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Intrasplenic Thymus Organogenesis from Injectable Tissue Fragments Restores Functional T-Cell Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Paraventricular oxytocin neurons attenuate post-ischemic brain injury by suppressing microglia-mediated neuroinflammation.Cell communication and signaling : CCS · 2026Article
- Limited nesting stress in mice as a model to study neuroimmune relationships in postpartum depression.Journal of neuroendocrinology · 2026Article
- Effects of occupational stress on the distribution of circulating T lymphocyte subsets and psychological health of young anaesthesiologists.BMC psychology · 2025Article
- Oxytocin-Mediate Modulation of Splenic Immunosuppression in Chronic Social Stress Through Neuroendocrine Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Chronic social stress (CSS) is a significant public health challenge that negatively impacts behavior and immune function through brain-spleen interactions. Oxytocin (OT), a neuropeptide critical for social behavior and immune regulation, is upregulated during CSS, though its underlying mechanisms remain unclear. This study investigates the role of OT in splenic immune modulation using a murine model of CSS. Behavioral evaluations, serum oxytocin quantification, and splenic immunophenotypic analysis were performed. Splenic denervation confirmed OT's neuromodulatory role, whereas OTR antagonism revealed its endocrine function. CSS-induced OT elevation was associated with immunosuppression, characterized by increased Foxp3⁺ regulatory T cells and reduced CD4⁺ T and CD19⁺ B cells. OT also modulated macrophage polarization, inhibiting M1-like (pro-inflammatory) and enhancing M2-like (anti-inflammatory) phenotypes. Denervation or pharmacological blockade of OT signaling partly reversed CSS-induced splenic immunosuppression but adversely affected survival in CSS-exposed mice. Additionally, denervation or OTR antagonism reduced the mice's response to social defeat, as shown by decreased social avoidance behavior. These findings suggest that OT-mediated immunosuppression likely represents a compensatory mechanism in response to chronic social stress. Targeting the OT-immune axis could offer innovative therapeutic approaches for stress-associated disorders by restoring immune homeostasis while maintaining behavioral integrity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.