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      The regulation of inflammation by interferons and their STATs

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          Abstract

          Interferons (IFN) are subdivided into type I IFN (IFN-I, here synonymous with IFN-α/β), type II (IFN-γ) and type III IFN (IFN-III/IFN-λ) that reprogram nuclear gene expression through STATs 1 and 2 by forming STAT1 dimers (mainly IFN-γ) or the ISGF3 complex, a STAT1-STAT2-IRF9 heterotrimer (IFN-I and IFN-III). Dominant IFN activities in the immune system are to protect cells from viral replication and to activate macrophages for enhanced effector function. However, the impact of IFN and their STATs on the immune system stretches far beyond these activities and includes the control of inflammation. The goal of this review is to give an overview of the different facets of the inflammatory process that show regulatory input by IFN/STAT.

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          Origin and physiological roles of inflammation.

          Ruslan Medzhitov (2008)
          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Development of monocytes, macrophages, and dendritic cells.

            Frederic Geissmann, Markus Manz, Steffen Jung … (2010)
            Monocytes and macrophages are critical effectors and regulators of inflammation and the innate immune response, the immediate arm of the immune system. Dendritic cells initiate and regulate the highly pathogen-specific adaptive immune responses and are central to the development of immunologic memory and tolerance. Recent in vivo experimental approaches in the mouse have unveiled new aspects of the developmental and lineage relationships among these cell populations. Despite this, the origin and differentiation cues for many tissue macrophages, monocytes, and dendritic cell subsets in mice, and the corresponding cell populations in humans, remain to be elucidated.
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              Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus.

              E. Baechler, F Batliwalla, G Karypis … (2003)
              Systemic lupus erythematosus (SLE) is a complex, inflammatory autoimmune disease that affects multiple organ systems. We used global gene expression profiling of peripheral blood mononuclear cells to identify distinct patterns of gene expression that distinguish most SLE patients from healthy controls. Strikingly, about half of the patients studied showed dysregulated expression of genes in the IFN pathway. Furthermore, this IFN gene expression "signature" served as a marker for more severe disease involving the kidneys, hematopoetic cells, and/or the central nervous system. These results provide insights into the genetic pathways underlying SLE, and identify a subgroup of patients who may benefit from therapies targeting the IFN pathway.
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                Author and article information

                Journal
                Journal ID (nlm-ta): JAKSTAT
                Journal ID (iso-abbrev): JAKSTAT
                Journal ID (publisher-id): JKST
                Title: JAK-STAT
                Publisher: Landes Bioscience
                ISSN (Print): 2162-3988
                ISSN (Electronic): 2162-3996
                Publication date (Print): 01 January 2013
                Publication date (Electronic): 01 January 2013
                Publication date PMC-release: 01 January 2013
                Volume: 2
                Issue: 1
                Electronic Location Identifier: e23820
                Affiliations
                [1 ]Max F. Perutz Laboratories; University of Vienna; Vienna, Austria
                [2 ]Institute of Animal Breeding and Genetics and Biomodels Austria; University of Veterinary Medicine Vienna; Vienna, Austria
                Author notes
                [* ]Correspondence to: Thomas Decker; Email: thomas.decker@ 123456univie.ac.at
                Article
                Publisher ID: 2013JAKS0133R Publisher Item ID: 23820
                DOI: 10.4161/jkst.23820
                PMC ID: 3670275
                PubMed ID: 24058799
                SO-VID: 30733f29-5ca4-4aca-a189-7f9b20a4d19a
                Copyright © Copyright © 2013 Landes Bioscience
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                Date received : 22 January 2013
                Date revision received : 29 January 2013
                Date accepted : 29 January 2013
                Categories
                Subject: Special Focus Review

                Keywords: interferon,stat,inflammation,leukocyte,chemokine,nitric oxide,inflammasome,autoimmune
                Data availability:
                Keywords: interferon, stat, inflammation, leukocyte, chemokine, nitric oxide, inflammasome, autoimmune

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