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The following is a summary of “Causal role of immune cells in bipolar disorder: a Mendelian randomization study,” published in the August 2024 issue of Psychiatry by Wang et al.
Recent advances in high-density genetic markers and genome-wide association studies have improved understanding of the immunological mechanisms behind bipolar disorder (BD).
Researchers conducted a retrospective study on how immune cells influence the risk of BD, as current studies are limited.
They performed a bidirectional 2-sample Mendelian Randomization (MR) analysis to examine the causal link between BD and immune cell morphologies. Immune cell traits were obtained from a cohort of Sardinian research, while GWAS summary statistics for BD came from the Psychiatric Genomics Consortium. The analysis included sensitivity checks, with MR-Egger and MR-Presso methods employed to detect horizontal pleiotropy. Cochran’s Q test assessed heterogeneity and adjusted results for the false discovery rate (FDR).
The result showed 6 immune cell phenotypes associated with BD incidence (P<0.01), which were IgD-CD27-% lymphocyte, CD33br HLA DR+ CD14- AC, CD8 on CD28+ CD45RA+ CD8br, CD33br HLA DR+ AC, CD14 on CD14+ CD16+ monocyte, and HVEM on CD45RA- CD4+. After adjusting for a FDR of 0.2, only 2 phenotypes remained statistically significant including IgD-CD27-% lymphocyte (OR=1.099, 95% CI: 1.051-1.149, P=3.51E-05, FDR=0.026) and CD33br HLA DR+ CD14- AC (OR=0.981, 95% CI: 0.971-0.991, P=2.17E-04, FDR=0.079). In reverse MR analysis, BD notably impacted 4 monocyte phenotypes (P<0.01): CD64 on CD14+ CD16+ monocyte, CD64 on monocyte, CX3CR1 on CD14- CD16-, and CD64 on CD14+ CD16- monocyte. No results were statistically significant after applying FDR correction (FDR<0.2).
Investigators concluded that the MR study highlighted associations between immune cell phenotypes, genetics, and BD, offering new insights for potential therapeutic targets.
Source: frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2024.1411280/abstract
