Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Causal Relationship Between Post-Traumatic Stress Disorder and Immune Cell Traits: A Mendelian Randomization Study.

Abstract

INTRODUCTION: Post-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. METHODS: To 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. RESULTS: For 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. CONCLUSION: The 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.