This study investigates the causal relationship between immune cell traits and generalized anxiety disorder (GAD) using a two-sample Mendelian randomization (MR) analysis. The research utilized genetic data from the FinnGen dataset and the GWAS catalog to examine 731 immune cell traits, including morphological parameters, median fluorescence intensity, absolute cell counts, and relative cell counts. The study performed both forward and reverse MR analyses to assess the causal effects of immune cell traits on GAD and vice versa. Results showed that GAD had no statistically significant effect on immunophenotypes after adjusting for false discovery rate (FDR). However, several immune cell traits were associated with GAD, including decreased PB/PC levels in B cells, reduced PB/PC absolute counts in GAD patients, and diminished PB/PC levels in lymphocytes. Additionally, GAD was found to have a causal effect on certain immune cell traits, such as CD27 on IgD-CD38br, CD20-%B cell, and FSC-A levels on granulocytes. The study also identified two lymphocyte subsets significantly associated with GAD risk: CD24+ CD27+ B cells and CD28+ CD4+ T cells. The findings suggest a potential link between immune cell traits and GAD, highlighting the importance of immune system regulation in the pathogenesis of the disorder. The study provides insights into the biological mechanisms underlying GAD and offers a foundation for future clinical research. The results were robust, with no evidence of horizontal pleiotropy, and were validated through sensitivity analyses. The study underscores the role of immune cells in GAD and suggests that further research is needed to explore the underlying biological pathways and potential therapeutic targets.This study investigates the causal relationship between immune cell traits and generalized anxiety disorder (GAD) using a two-sample Mendelian randomization (MR) analysis. The research utilized genetic data from the FinnGen dataset and the GWAS catalog to examine 731 immune cell traits, including morphological parameters, median fluorescence intensity, absolute cell counts, and relative cell counts. The study performed both forward and reverse MR analyses to assess the causal effects of immune cell traits on GAD and vice versa. Results showed that GAD had no statistically significant effect on immunophenotypes after adjusting for false discovery rate (FDR). However, several immune cell traits were associated with GAD, including decreased PB/PC levels in B cells, reduced PB/PC absolute counts in GAD patients, and diminished PB/PC levels in lymphocytes. Additionally, GAD was found to have a causal effect on certain immune cell traits, such as CD27 on IgD-CD38br, CD20-%B cell, and FSC-A levels on granulocytes. The study also identified two lymphocyte subsets significantly associated with GAD risk: CD24+ CD27+ B cells and CD28+ CD4+ T cells. The findings suggest a potential link between immune cell traits and GAD, highlighting the importance of immune system regulation in the pathogenesis of the disorder. The study provides insights into the biological mechanisms underlying GAD and offers a foundation for future clinical research. The results were robust, with no evidence of horizontal pleiotropy, and were validated through sensitivity analyses. The study underscores the role of immune cells in GAD and suggests that further research is needed to explore the underlying biological pathways and potential therapeutic targets.