Fig. 1: Neuroimmunological mechanisms of depression.
From: Modulation of neuroimmune cytokine networks by antidepressants: implications in mood regulation
This figure depicts the interplaybetween the immune system and central nervous system (CNS) homeostasis. Disruption of the blood-brain barrier (BBB) increases brain access to immune cells and cytokines, activating microglia and promoting neuroinflammation. Similarly, peripheral inflammation, driven by immune cell activation and the release of peripheral cytokines (e.g., IL-1β, IL-6, TNF-α, IFN-γ) further contribute by altering vascular permeability and crossing or signaling to the brain. IFN-γ also activates IDO, diverting tryptophan from serotonin to neurotoxic kynurenine metabolites (e.g., 3-HK, QA), which are implicated in depressive symptoms. IDO Indoleamine 2,3-dioxygenase, IFN-γ Interferon-gamma, TNF-α Tumor Necrosis Factor-alpha, IL Interleukin, QA Quinolinic Acid, 3-HK 3-Hydroxykynurenine, Treg Regulatory T cells, CREB cAMP response element-binding protein, Htr1b 5-Hydroxytryptamine Receptor 1B. Created with BioRender (www.BioRender.com).
