After the immune response system is activated, the human body will release proinflammatory cytokines, causing neuroendocrine and neurobiological changes, and IL-1, IL-6, and other factors can reduce neuroplasticity by directly stimulating the hypothalamic-pituitary-adrenal axis and accelerate tryptophan breakdown, the precursor substance of 5-hydroxytryptamine, thus participating in the pathogenesis of depression [19, 20]. This evidence concerns the gene IL1B and major depressive disorder.