ArticleBrain and behavior2024
Causal Relationship Between Post-Traumatic Stress Disorder and Immune Cell Traits: A Mendelian Randomization Study.
Article in Brain and behavior, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Biological treatments for co-occurring eating disorders and psychological trauma: a systematic review.Frontiers in psychiatry · 2025Pooled it
- The gut microbiota-immune-brain axis in post-traumatic stress disorder: mechanistic integration and translational prospects.Frontiers in immunology · 2026Review
- Exploring Chronic Pain, Immune Dysfunction and Lifestyle: A Focus on T Cell Exhaustion and Senescence.Biomolecules · 2025Review
- Research Progress on Inflammation and Immune Dysregulation in PTSD.Brain and behavior · 2025Review
- A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases.Translational psychiatry · 2025Article
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Authors and funding
4 authors.
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Abstract
introductionPost-traumatic stress disorder (PTSD) is a debilitating psychological disorder that occurs after exposure to catastrophic-level experiences. Although alterations in immune function have been identified in individuals with PTSD, the causal relationship between the two remains unclear.
methodsTo investigate the causal relationship between PTSD and immune function, we conducted the forward and backward two-sample Mendelian randomization (MR) analyses, based on summary-level genome-wide association studies (GWAS) data on PTSD and immune cell traits.
resultsFor the forward MR analysis, PTSD was found to reduce the levels of CD62L- dendritic cell (DC) (beta = -0.254, FDR = 0.01), CD86+ myeloid DC (beta = -0.238, FDR = 0.014), CD62L- myeloid DC (beta = -0.26, FDR = 0.01), CD62L- CD86+ myeloid DC absolute count (beta = -0.264, FDR = 0.024), and CD62L- CD86+ myeloid DC (beta = -0.328, FDR = 0.002). In contrast, PTSD was observed to increase the level of CD28- CD8dim T-cell absolute count (beta = 0.27, FDR = 0.029). For the backward MR analysis, the odds ratio (OR) for CD33 on CD33dim HLA DR+ CD11b- in relation to PTSD risk was found to be 1.045 (95% CI = 1.021-1.069, FDR = 0.008). The OR for FSC-A on HLA DR+ CD8br was 1.048 (95% CI = 1.018-1.079, FDR = 0.039) and for CCR2 on CD14- CD16+ monocyte was 1.059 (95% CI = 1.027-1.092, FDR = 0.008). No significant pleiotropy was detected in both forward and backward MR analyses.
conclusionThe bidirectional MR study shed light on the intricate interplay between immune function and PTSD. The identification of a bidirectional causal relationship between T cells and PTSD opens new avenues for considering innovative approaches to the prevention and early intervention of PTSD.
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