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Context: The aim of this review was to address the recent data regarding the role of IL-17A in the pathogenesis of depression and its complications, such as cancer. Evidence Acquisition: This review article summarizes the recent data on the role of IL-17A in depression, using the PubMed and Google Scholar databases. Results: It has been documented that depression may alter the immune response via unknown mechanism/s. It is possible that immune responses and depression are linked via several molecules, including cytokines. IL-17A, a pro-inflammatory cytokine, participates in the pathogenesis of several inflammatory-based diseases, such as autoimmunity. Conclusions: Due to the comorbidity of depression and chronic inflammatory processes, and depression’s effect on the immune system, it may be hypothesized that the IL-17A cytokine plays a key role in the pathogenesis of depression.

BACKGROUND NF-kB is a transcription factor that is a downstream target of several cell signaling systems including TLRs. Defective expression of the molecule can lead to inappropriate immune responses. Previous studies revealed that depression can affect immune responses, but its molecular mechanisms are yet to be fully understood. Thus, the main aim of this study was to identify if mRNA levels of NF-kB are changed in the PBMCs isolated from Iranian depressed medical students. METHODS This cross-sectional study was done on 38 Iranian depressed medical students and 43 healthy students as a control group. The mRNA levels of NF-kB were assessed in parallel with beta-actin (as the housekeeping gene) using Real-Time PCR technique. RESULTS Our results showed that mRNA levels of NF-kB were significantly decreased in isolated PBMCs from depressed patients compared to healthy controls. CONCLUSIONS According to the results obtained in the present study, it seems that depressed patients are unable to appropriately express NF-kB at mRNA levels which may in turn lead to defective molecule expression.