The role of IL-17 secretion in mediating the influence of stress on cancer and other human systemic diseases

Abstract

Several experimental and clinical investigations have shown that stress may predispose to the most severe systemic illnesses, including cancer and autoimmune diseases.1 According to the recent discoveries of the Psycho-neuroendocrino-immunology (PNEI),2 cancer-and autoimmunity-related immune alterations may depend at least at the beginning of disease on an altered psychoneuroendocrine regulation of the immune responses. From an immune point of view, despite the great complexity of immune interactions involved in the onset of human systemic diseases, cancer and autoimmunity may be considered as the result of two opposite manners of immune reaction, consisting of a deficiency in the immune response in cancer and an exaggerated reaction in the autoimmunity, which allows a consequent reaction also against self-antigens. More in detail, the differences in the immune behavior occurring in cancer and in autoimmune diseases would synthetically depend on the different interactions among the three main subsets of CD4+T lymphocytes, consisting of T helper (TH) (CD4+CD25-CD17-), regulatory T lymphocytes (T reg) (CD4+CD25+) and TH-17 lymphocytes (CD4+CD17+).3–5 In particular, T reg cell number and function have been shown to be abnormally high in cancer and abnormally low in the autoimmunity.3–6