The untold story of IFN-γ in cancer biology. (October 2016)
- Record Type:
- Journal Article
- Title:
- The untold story of IFN-γ in cancer biology. (October 2016)
- Main Title:
- The untold story of IFN-γ in cancer biology
- Authors:
- Kursunel, M. Alper
Esendagli, Gunes - Abstract:
- Highlights: This review highlights the regulatory functions of interferon (IFN)-γ in cancer biology. IFN-γ is acknowledged with its cytostatic, pro-apoptotic and immune-provoking effects against tumor development. Many regulatory pathways can be induced by IFN-γ, to protect the normal tissues from collateral damage and to facilitate the re-establishment of homeostasis. Malignant cells take the advantage of IFN-γ as an inducer of mediators inhibiting anti-tumor immune reactions. Under the influence of tumor-derived factors, certain types of immune cells are also licensed by IFN-γ to perform regulatory actions. A better understanding of the alternative functions of IFN-γ will provide new insights for cancer biology and immune intervention therapies. Abstract: Interferon (IFN)-γ is the uppermost cytokine implicated in anti-tumor immunity. With its cytostatic, pro-apoptotic and immune-provoking effects, IFN-γ 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-γ-mediated immunity for different types of cancer. However, the outcomes were not satisfactory and leaded to questioning of alternative actions of IFN-γ. Many regulatory pathways can be induced by IFN-γ to protect the normal tissues from collateral damage and to facilitate the re-establishment of homeostasis. Nevertheless, malignant cells canHighlights: This review highlights the regulatory functions of interferon (IFN)-γ in cancer biology. IFN-γ is acknowledged with its cytostatic, pro-apoptotic and immune-provoking effects against tumor development. Many regulatory pathways can be induced by IFN-γ, to protect the normal tissues from collateral damage and to facilitate the re-establishment of homeostasis. Malignant cells take the advantage of IFN-γ as an inducer of mediators inhibiting anti-tumor immune reactions. Under the influence of tumor-derived factors, certain types of immune cells are also licensed by IFN-γ to perform regulatory actions. A better understanding of the alternative functions of IFN-γ will provide new insights for cancer biology and immune intervention therapies. Abstract: Interferon (IFN)-γ is the uppermost cytokine implicated in anti-tumor immunity. With its cytostatic, pro-apoptotic and immune-provoking effects, IFN-γ 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-γ-mediated immunity for different types of cancer. However, the outcomes were not satisfactory and leaded to questioning of alternative actions of IFN-γ. Many regulatory pathways can be induced by IFN-γ 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-γ 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-γ to perform regulatory actions. This review focuses on the immune modulatory functions of IFN-γ in cancer as an alternative story to be told. … (more)
- Is Part Of:
- Cytokine & growth factor reviews. Volume 31(2016)
- Journal:
- Cytokine & growth factor reviews
- Issue:
- Volume 31(2016)
- Issue Display:
- Volume 31, Issue 2016 (2016)
- Year:
- 2016
- Volume:
- 31
- Issue:
- 2016
- Issue Sort Value:
- 2016-0031-2016-0000
- Page Start:
- 73
- Page End:
- 81
- Publication Date:
- 2016-10
- Subjects:
- APC antigen presenting cell -- CD cluster of differentiation -- COX cyclooxygenase -- CTLA-4 cytotoxic T-lymphocyte antigen-4 -- CTL cytotoxic T lymphocyte -- DC dendritic cell -- IDO indoleamine 2, 3-dioxygenase -- iNOS inducible nitric oxide synthase -- IFN interferon -- IL interleukin -- IRF interferon regulatory factor -- LAG3 lymphocyte activation gene -- MDSC myeloid-derived suppressor cell -- MHC major histocompatibility complex -- NF-κB nuclear factor-kappa B -- NK natural killer -- NO and nitric oxide -- PG prostaglandin -- PD-1 programmed cell death-1 -- PD-L programmed cell death-ligand -- ROS reactive oxygen species -- STAT signal transducers and activators of transcription -- TCR T cell receptor -- TGF-β transforming growth factor -- Th T helper -- TIM-3 T-cell immunoglobulin and mucin domain-containing protein-3 -- TRAIL TNF-related apoptosis-inducing ligand -- Treg regulatory T cell
Interferon -- Cancer -- T cell -- Myeloid cell -- Immune regulation -- Anti-tumor immunity -- Immunotherapy
Cytokines -- Periodicals
571.84 - Journal URLs:
- http://www.sciencedirect.com/science/journal/13596101 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.cytogfr.2016.07.005 ↗
- Languages:
- English
- ISSNs:
- 1359-6101
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3506.778500
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