In addition, long-term exposure to high concentrations of IL-6, also characteristic of depression [20,21], increases the production of IL-17 by Th17 lymphocytes and additionally reduces corticoid inhibitory effects on activated T cells [167], and the use of anti-IL-6R restored the ability of hydrocortisone to inhibit both T-cell proliferation and IL-17 production. This evidence concerns the gene IL17A and major depressive disorder.