Following reports that IL-36 beta could amplify Th1 responses in CD4+ T cells [37], a number of studies have shown the induction of IL-36 cytokine expression, especially IL-36 gamma, in response to infections including pneumonia, herpes simplex virus (HSV), and candidiasis [68,69,70,71,72,73], suggesting that IL-36 cytokines may play a significant role in host immunity. This evidence concerns the gene CD4 and candidiasis.