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Direct effects of type I interferons on cells of the immune system.
- Source :
-
Clinical cancer research : an official journal of the American Association for Cancer Research [Clin Cancer Res] 2011 May 01; Vol. 17 (9), pp. 2619-27. Date of Electronic Publication: 2011 Mar 03. - Publication Year :
- 2011
-
Abstract
- Type I interferons (IFN-I) are well-known inducers of tumor cell apoptosis and antiangiogenesis via signaling through a common receptor interferon alpha receptor (IFNAR). IFNAR induces the Janus activated kinase-signal transducer and activation of transcription (JAK-STAT) pathway in most cells, along with other biochemical pathways that may differentially operate, depending on the responding cell subset, and jointly control a large collection of genes. IFNs-I were found to systemically activate natural killer (NK) cell activity. Recently, mouse experiments have shown that IFNs-I directly activate other cells of the immune system, such as antigen-presenting dendritic cells (DC) and CD4 and CD8 T cells. Signaling through the IFNAR in T cells is critical for the acquisition of effector functions. Cross-talk between IFNAR and the pathways turned on by other surface lymphocyte receptors has been described. Importantly, IFNs-I also increase antigen presentation of the tumor cells to be recognized by T lymphocytes. These IFN-driven immunostimulatory pathways offer opportunities to devise combinatorial immunotherapy strategies.<br /> (©2011 AACR.)
- Subjects :
- Animals
Antigen-Presenting Cells drug effects
Antigen-Presenting Cells immunology
Cells immunology
Humans
Mice
Models, Biological
Signal Transduction drug effects
Signal Transduction physiology
T-Lymphocytes drug effects
T-Lymphocytes immunology
Cells drug effects
Immune System drug effects
Interferon Type I pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1557-3265
- Volume :
- 17
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- Clinical cancer research : an official journal of the American Association for Cancer Research
- Publication Type :
- Academic Journal
- Accession number :
- 21372217
- Full Text :
- https://doi.org/10.1158/1078-0432.CCR-10-1114