Literature DB >> 12890422

Anti-inflammatory properties of pro-inflammatory interferon-gamma.

Heiko Mühl1, Josef Pfeilschifter.   

Abstract

Production of interferon-gamma (IFNgamma) in response to infection is a hallmark of innate and adaptive immunity. In addition to the pivotal role of IFNgamma in host defense, its excessive release has been associated with the pathogenesis of chronic inflammatory and autoimmune diseases. In fact, knockout models reveal that IFNgamma plays a key role in mediating a number of pathological processes related to chronic immune activation. On the other hand, evidence has been accumulated in recent years that supports the concept of a dual role of IFNgamma in inflammation. Here, we review anti-inflammatory aspects of IFNgamma in the regulatory network of cytokine biology. These include induction of anti-inflammatory molecules such as interleukin (IL)-1 receptor antagonist (IL-1Ra) and IL-18 binding protein (IL-18BP), modulation of pro-inflammatory cytokine production, activation of apoptosis, and interference with the signal transduction machinery by induction of suppressors of cytokine signaling (SOCS).

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Year:  2003        PMID: 12890422     DOI: 10.1016/S1567-5769(03)00131-0

Source DB:  PubMed          Journal:  Int Immunopharmacol        ISSN: 1567-5769            Impact factor:   4.932


  89 in total

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4.  The integrated stress response prevents demyelination by protecting oligodendrocytes against immune-mediated damage.

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7.  IL-36γ/IL-1F9, an innate T-bet target in myeloid cells.

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8.  Mice with a selective impairment of IFN-gamma signaling in macrophage lineage cells demonstrate the critical role of IFN-gamma-activated macrophages for the control of protozoan parasitic infections in vivo.

Authors:  Jennifer E Lykens; Catherine E Terrell; Erin E Zoller; Senad Divanovic; Aurelien Trompette; Christopher L Karp; Julio Aliberti; Matthew J Flick; Michael B Jordan
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9.  Enhanced integrated stress response promotes myelinating oligodendrocyte survival in response to interferon-gamma.

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10.  IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like skin inflammation.

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Journal:  J Clin Invest       Date:  2008-02       Impact factor: 14.808

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