Heumann Jens, Cole Steve W, Eisner Manuel, Ribeaud Denis, Grünblatt Edna, Shanahan Michael J
Jacobs Center for Productive Youth Development, University of Zurich, 8050, Zurich, Switzerland.
Department of Sociology, University of Zurich, 8050, Zurich, Switzerland.
Brain Behav Immun Health. 2025 May 29;48:101025. doi: 10.1016/j.bbih.2025.101025. eCollection 2025 Oct.
Adolescents who experience peer victimization (PV) often report psychosomatic complaints; however, little is known about possible underlying molecular effects. Social adversity has already been shown to downregulate immune genes and upregulate inflammatory genes. This study investigated PV for potentially enduring molecular effects, in terms of gene expression, leukocyte composition, and cytokine levels in young adulthood. Participants ( = 144; 47% female) were drawn from the Zurich Brain and Immune Gene Study (z-GIG). PV was studied from age 11 to 20, and molecular data were collected at age 22. A counterfactual framework with genetically informed inverse probability weighting was applied to account for individual and environmental confounders. Compared to non-PV controls, victims showed extensive immune changes. deconvolution revealed shifts in leukocyte composition, including an M2-like monocyte-skewed profile. Differentially expressed genes were enriched in several Reactome pathways, including , , , , and . Transcription factors STAT2 and IRF2 emerged as key regulators, with target genes primarily in the and pathways. Cytokine levels also differed, including elevated pro-inflammatory markers such as CCL4, TNF, CXCL9, and CXCL10. The findings provide preliminary evidence of the immunomodulatory potential of PV and highlight the importance of public health strategies aimed at prevention, building resilience, and mitigating long-term effects.
经历同伴侵害(PV)的青少年经常报告有身心方面的不适;然而,对于可能的潜在分子效应却知之甚少。社会逆境已被证明会下调免疫基因并上调炎症基因。本研究调查了青少年期同伴侵害在成年早期对基因表达、白细胞组成和细胞因子水平方面可能产生的持久分子效应。参与者(n = 144;47%为女性)来自苏黎世大脑与免疫基因研究(z - GIG)。对同伴侵害的研究时间跨度为11岁至20岁,并在22岁时收集分子数据。采用了具有遗传信息的逆概率加权的反事实框架来考虑个体和环境混杂因素。与未经历同伴侵害的对照组相比,受害者表现出广泛的免疫变化。去卷积分析揭示了白细胞组成的变化,包括类似M2型的单核细胞偏向性特征。差异表达基因在几个Reactome通路中富集,包括……、……、……、……和……。转录因子STAT2和IRF2成为关键调节因子,其靶基因主要参与……和……通路。细胞因子水平也存在差异,包括促炎标志物如CCL4、TNF、CXCL9和CXCL10升高。这些发现为同伴侵害的免疫调节潜力提供了初步证据,并突出了旨在预防、增强恢复力和减轻长期影响的公共卫生策略的重要性。