The untold story of IFN-gamma in cancer biology

KURŞUNEL M. A., ESENDAĞLI G.

CYTOKINE & GROWTH FACTOR REVIEWS, cilt.31, ss.73-81, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 31
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1016/j.cytogfr.2016.07.005
  • Dergi Adı: CYTOKINE & GROWTH FACTOR REVIEWS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.73-81
  • Anahtar Kelimeler: Interferon, Cancer, T cell, Myeloid cell, Immune regulation, Anti-tumor immunity, Immunotherapy, T-CELL THERAPY, NATURAL-KILLER-CELL, MHC CLASS-II, TUMOR-INFILTRATING LYMPHOCYTES, MACROPHAGE ACTIVATION SYNDROME, INDEPENDENT PROGNOSTIC-FACTOR, RECOMBINANT INTERFERON-GAMMA, METASTATIC MELANOMA PATIENTS, ANTITUMOR IMMUNE-RESPONSES, CYTOKINE RELEASE SYNDROME
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Interferon (IFN)-gamma is the uppermost cytokine implicated in anti-tumor immunity. With its cytostatic, proapoptotic and immune-provoking effects, IFN-gamma plays a central role in the recognition and elimination of transformed cells. Considering well-characterized anti-tumor effects of this cytokine, many clinical trials and immunotherapy approaches have been designed to reinforce IFN-gamma-mediated immunity for different types of cancer. However, the outcomes were not satisfactory and leaded to questioning of alternative actions of IFN-gamma. Many regulatory pathways can be induced by IFN-gamma to protect the normal tissues from collateral damage and to facilitate the re-establishment of homeostasis. Nevertheless, malignant cells can take the advantage of IFN-gamma as an inducer of mediators inhibiting anti-tumor immune reactions. In addition, under the influence of tumor-derived factors, certain types of immune cells are also licensed by IFN-gamma to perform regulatory actions. This review focuses on the immune modulatory functions of IFN-gamma in cancer as an alternative story to be told. (C) 2016 Elsevier Ltd. All rights reserved.