Background: Immune system plays an important role in brain
development and function. With the discovery of increased circulating inflammatory
cytokine levels in depression over two decades ago, evidence implicating immune
system alterations in the disease has increasingly accumulated.
Objective: To assess the underlying etiology and pathophysiology, a brief overview
of the hypothesis free genomic, transcriptomic and proteomic studies in depression is
presented here in order to specifically examine if the immune and inflammation
hypothesis of depression is supported.
Results: It is observed that genes identified in genome-wide association studies, and
genes showing differential expression in transcriptomic studies in human depression
do separately overrepresent processes related to both development as well as functioning of the immune
system, and inflammatory response. These processes are also enriched in differentially expressed genes
reported in animal models of antidepressant treatment. It is further noted that some of the genes identified in
genome sequencing and proteomic analyses in human depression, and transcriptomic studies in chronic social
defeat stress, an established animal model of depression, relate to immune and inflammatory pathways.
Conclusion: In conclusion, integrative genomics evidence supports the immune and inflammation
hypothesis of depression.