Mechanisms of type I interferon signaling in normal and malignant cells

• Authors: Y. Li , K.K. Srivastava , L.C. Platanias
• Languages of publication: EN

Abstracts

EN

Type I interferons (IFNs) are cytokines that induce multiple biological effects on target cells, including antiviral, antiproliferative, and immunomodulatory activities. Consistent with the pleiotropic nature of these cytokines, multiple signaling pathways are activated during binding of IFNs to the type I IFN receptor. An important signaling cascade activated by type I IFNs is the Jak-Stat pathway. Activation of the Tyk-2 and Jak-1 kinases, and downstream formation of various Stat complexes, mediates IFN-dependent gene transcription for IFN-stimulated genes. In addition to the classic Jak-Stat pathway, type I IFNs activate multiple other pathways, including the insulin receptor substrate-phosphatidylinositol 3'-kinase cascade, the CBL-CrkL pathway, and mitogen-activated protein kinase pathways. There is accumulating evidence that non-Stat IFN-regulated signaling pathways play important roles in the generation of the antiproliferative effects of type I IFNs. In this review, the regulation of various signaling cascades by the type I IFN receptor is summarized and an update on recent advances in the field is provided.

Keywords

EN

CYTOKINE; INTERFERON; MALIGNAT CELL; SIGNALING

Discipline

• IMMUNOLOGY: IMMUNOLOGY

• Publisher: Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences
• Journal: Archivum Immunologiae et Therapiae Experimentalis
• Year: 2004
• Volume: 52
• Issue: 3
• Pages: 156-163

Contributors

author

Y. Li

author

K.K. Srivastava

author

L.C. Platanias

• Document Type: ARTICLE
• Publication order reference: Leonidas C. Platanias, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical School, 710 North Fairbanks Court, Olson 8250, Chicago, IL 60611, USA