Immunity and autoimmunity: revising the concepts of response to breast cancer

Abstract

Evading immune destruction should be considered an emerging hallmark of cancer. Highly immunogenic cancer cells can be eliminated in immunocompetent hosts as a result of the "immunoediting" process. Weakly immunogenic variants can grow and generate solid tumors. Regulatory T cells (Tregs) were found to be involved in the maintenance of the immune tolerance both preventing autoimmune disease and curtailing antitumour immune response. Modulation of immune response in cancer patients is the result of a balanced activity of Tregs and T effector cells. In cancer patients increased number of Tregs was found in blood and tumour tissue: it was demonstrated that Tregs suppress T-cell response and natural killer (NK) cells proliferation and function, thus interfering both with acquired and innate immunity. Upregulation of Tregs in tumor bed can be associated with worse prognosis. Drugs blocking function of Tregs increase activity of T effectors and, as side effect, induce an autoimmune disease. Issues of biology and prognosis of breast cancer in the presence of a deregulation of the immune system needs to be studied. The identification of immunological and genetic features affecting immune response in patients with minimal tumor burden are the optimal background for development of clinical studies in the adjuvant setting.