ReviewJournal of neuroinflammation2026
Neuroimmune programming of childhood trauma: comorbid mechanisms and developmental origins of depression and autoimmune diseases.
Review in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- The mediating role of the aggregate index of systemic inflammation between childhood emotional neglect and depressive severity in major depressive disorder: a cross-sectional study.Frontiers in psychiatry · 2026Article
- Childhood adversity and autoimmune diseases: global research landscape, immune-related hotspots, and emerging trends from a bibliometric analysis of three databases.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adverse childhood experiences (ACEs) represent a critical environmental trigger for the adult comorbidity of depression and autoimmune diseases. This review synthesizes evidence showing that ACEs induce persistent dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system, thereby promoting a chronic low-grade inflammatory state. This state is characterized by elevated pro-inflammatory cytokines (e.g., IL-6, TNF-α), immune cell dysfunction, and epigenetic modifications. Facilitated by microglial activation and monocyte-mediated disruption of the blood–brain barrier, this pro-inflammatory milieu disrupts central nervous system homeostasis, contributing to the pathogenesis of both depressive symptoms and autoimmune disorders. Aberrant neuroimmune crosstalk emerges as a core mechanism underlying this comorbidity. Future research must delineate developmental windows of vulnerability and the differential effects of adversity types to translate these insights into novel therapeutic strategies targeting the neuroimmune axis—such as anti-cytokine therapies or vagus nerve stimulation—for high-risk populations.
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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.