Современная онкология (Mar 2015)

Breast cancer immunology: theory and prospects (review)

  • I V Kolyadina,
  • I V Poddubnaya

Journal volume & issue
Vol. 17, no. 1
pp. 12 – 18

Abstract

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This review deals with the detail presentation of the antitumor immunity basic mechanisms, of the interpretation of HLA class I and II histocompatibility genes - markers of the antigen-activated lymphocytes in the antigenic activation of lymphocytes and the role of T-cells (CD8+ T-killer cells and CD4+ T-helper cells) and NK cells in the realization of antitumor responses. We have described the unique mechanisms of cooperative humoral and cellular antitumor immunity - antibody-dependent cell-mediated cytotoxicity, and have evaluated its role in antitumor protecting the body against cancer. Advantages of the antitumor immunity is the possibility of T-lymphocytes to recognize tumor antigens in histocompatibility molecules of HLA-class I and II and-NK-cells to kill tumor cells without expression of HLA-class I and to acting in antibody-dependent cell-mediated cytotoxicity. The mutated cells can avoid the immune surveillance and cells cloning, the basis of these mechanisms is important immune processes; tumor progression can occur as a result of immune system damage (imperfect antitumor immunity) or as a result of tumor "immune invisibility". The causes of imperfect antitumor immunity are: the loss of tumor presentation histocompatibility molecules of HLA-class I and II, leading to the inability to show T-cell cytotoxicity, the expression of HLA-E and HLA-G, leading to blockade of NK-cells activity, the presence of suppressor Foxp3 + regulatory lymphocytes in tumor, the development of immunological tolerance (sustainable "unresponsiveness" of the immune system) during tumor growth and dissemination. We have showed the perspective study directions of prognostic and predicting roles of the immune tumor characteristics: subpopulations of stromal and intratumoral TILs, the markers expression HLA class I and II histocompatibility genes and non-classical suppressor molecu- les of HLA-E and HLA-G and tumor-infiltrating Foxp3(+)-lymphocytes. The study of the cellular and molecular basis of immune mechanisms will help us better understand the carcinogenesis and will optimize the therapeutic strategy for BC.

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