ReviewCNS neuroscience & therapeutics2026
Interleukins in Major Depressive Disorder: Lessons From Autoimmune Diseases and Pathways to Clinical Translation.
Review in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Integrated Chemometric and Machine Learning Analysis Identifies Peripheral Biosignatures Distinguishing Major Depressive Disorder from Bipolar Disorder: A Translational Cross-Sectional Study.Medicina (Kaunas, Lithuania) · 2026Article
- Interleukins in Major Depressive Disorder: Lessons From Autoimmune Diseases and Pathways to Clinical Translation.CNS neuroscience & therapeutics · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMajor Depressive Disorder (MDD) is a leading cause of disability, and limitations of the monoamine hypothesis have driven the exploration of complementary models, including the inflammatory hypothesis. This hypothesis suggests that in a subset of patients, immune dysregulation, especially involving interleukins (ILs), contributes to depression. This review compares IL dysregulation in MDD and autoimmune diseases to identify common and unique inflammatory mechanisms for treatment. RESULTS AND
conclusionSome MDD patients exhibit chronic, low-grade inflammation both systemically (in blood) and centrally (in CSF and brain). They show elevated pro-inflammatory IL-6, IL-1β, and IL-18, with insufficient anti-inflammatory IL-10. This immune dysregulation affects key neurobiological processes (monoamine metabolism, HPA axis, neurogenesis), linking inflammation to depressive symptoms. MDD and autoimmune diseases share inflammatory mediators and signaling pathways, supporting these as therapeutic targets; however, MDD's inflammation is low-grade and innate driven, whereas autoimmune diseases have high-grade, adaptive immune responses to specific antigens. Successful anti-IL therapies in autoimmune conditions provide a roadmap for treating inflammation-driven depression. Translating these findings to practice requires a precision immune-psychiatry approach. Biomarkers like C-reactive protein and IL-6 can identify an inflammatory depression subtype, and patients may benefit from targeted immunomodulatory strategies, repurposed biologics, novel small molecules, or lifestyle interventions particularly if standard antidepressants fail.
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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 OpenQuestion graph.