ArticleJournal of advanced research2024
T helper-1 activation via interleukin-16 is a key phenomenon in the acute phase of severe, first-episode major depressive disorder and suicidal behaviors.
Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Activation of the interleukin-23/Th17 axis in major depression: a systematic review and meta-analysis.European archives of psychiatry and clinical neuroscience · 2025Pooled it
- The gut-brain axis and inflammatory mediators in suicide and mental disorders with high suicide rates: a review of current evidence.Dialogues in clinical neuroscience · 2026Review
- Unifying the hallmarks of major depression through neuroimmune-metabolic-oxidative (NIMETOX) dysregulation: a mechanistic systems framework.Cellular & molecular immunology · 2026Review
- Selective Anti-Inflammatory Actions of Curcumin on Cytokine Pathways in Major Depressive Disorder.Brain and behavior · 2026Article
- Peripheral immune-redox signatures associate with cortical network alterations in anhedonic depression.Molecular psychiatry · 2026Article
- Sunshine duration and episodes of mental disorders and the inverse effect modification by ambient temperature.BMC medicine · 2026Article
- Neuroimmune programming of childhood trauma: comorbid mechanisms and developmental origins of depression and autoimmune diseases.Journal of neuroinflammation · 2026Review
- Whole Blood Transcriptome Analysis in Female Adolescents With Depression Accompanied by Nonsuicidal Self-Injury and Suicide Attempt.Depression and anxiety · 2026Observational
- Differentiating Between Major Depressive Disorder and Bipolar Disorder.Advances in experimental medicine and biology · 2026Review
- Pro-inflammatory cytokines level in depressed patients with suicidal behaviour: a systematic review and meta-analysis.Annals of general psychiatry · 2025Article
- Monomeric CRP and negative acute phase proteins, but not pentameric CRP, as biomarkers of major depression and MDMD.Acta neuropsychiatrica · 2025Article
- CD4 + T lymphocyte and cytokine profiles in depressive disorders.BMC psychiatry · 2025Article
- Neuroimmune, metabolic and oxidative stress pathways in major depressive disorder.Nature reviews. Neurology · 2025Review
- The associations of suicidal ideation with psychopathology and inflammatory cytokines in patients with chronic schizophrenia.BMC psychiatry · 2025Article
- HHV-6 and EBV reactivation in relapsing remitting multiple sclerosis: Disability, progression, and inflammation links.iScience · 2025Article
- Rethinking Depression-Beyond Neurotransmitters: An Integrated Psychoneuroendocrineimmunology Framework for Depression's Pathophysiology and Tailored Treatment.International journal of molecular sciences · 2025Review
- Genetic Variants of Interleukin-8 and Interleukin-16 and Their Association with Cervical Cancer Risk.Life (Basel, Switzerland) · 2025Article
- Association of the Single Nucleotide Polymorphisms rs11556218, rs4778889, rs4072111, and rs1131445 of the Interleukin-16 Gene with Ovarian Cancer.International journal of molecular sciences · 2024Article
- In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and increased immune-associated neurotoxicity.Scientific reports · 2024Article
- Understanding the Biological Relationship between Migraine and Depression.Biomolecules · 2024Review
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune-inflammatory pathways in major depressive disorder are confined to the major dysmood disorder (MDMD) phenotype (Maes et al., 2022). No studies have addressed the immune profile of first episode MDMD (FE-MDMD).
methodsThis study investigated the immune profiles of 71 patients with the acute phase of first-episode major depressive disorder (FE-MDMD) and 40 healthy controls. We measured 48 cytokines/chemokines/growth factors, classical M1, alternative M2, T helper (Th)-1, Th-2, and Th-17 phenotypes, immune-inflammatory response system (IRS), compensatory immunoregulatory system (CIRS), and neuro-immunotoxicity profiles.
resultsFE-MDMD patients show significantly activated M1, M2, Th-1, IRS, CIRS, and neurotoxicity, but not Th-2 or Th-17, profiles compared to controls. FE-MDMD is accompanied by Th-1 polarization, while there are no changes in M1/M2 or IRS/CIRS ratios. The top single indicator of FE-MDMD was by far interleukin (IL)-16, followed at a distance by TRAIL, IL-2R, tumor necrosis factor (TNF)-β. The severity of depression and anxiety was strongly associated with IRS (positively) and Th-2 (inversely) profiles, whereas suicidal behavior was associated with M1 activation. Around 56-60% of the variance in depression, anxiety, and suicidal behavior scores was explained by IL-16, platelet-derived growth factor (PDGF) (both positively), and IL-1 receptor antagonist (inversely). Increased neurotoxicity is mainly driven by IL-16, TNF-α, TRAIL, IL-6, and chemokine (CCL2, CCL11, CXCL1, CXCL10) signaling. Antidepressant-treated patients show an increased IRS/CIRS ratio as compared with drug-naïve FE-MDMD patients.
conclusionsFE-MDMD is accompanied by positive regulation of the IRS mainly driven by Th-1 polarization and T cell activation (via binding of IL-16 to CD4), and TNF, chemokine, and growth factor signaling.
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