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About: Interferon is a(n) research topic. Over the lifetime, 28969 publication(s) have been published within this topic receiving 1219645 citation(s). The topic is also known as: IFN & interferons. more


Journal ArticleDOI: 10.1146/ANNUREV.IMMUNOL.15.1.749
Abstract: Interferons are cytokines that play a complex and central role in the resistance of mammalian hosts to pathogens. Type I interferon (IFN-alpha and IFN-beta) is secreted by virus-infected cells. Immune, type II, or gamma-interferon (IFN-gamma) is secreted by thymus-derived (T) cells under certain conditions of activation and by natural killer (NK) cells. Although originally defined as an agent with direct antiviral activity, the properties of IFN-gamma include regulation of several aspects of the immune response, stimulation of bactericidal activity of phagocytes, stimulation of antigen presentation through class I and class II major histocompatibility complex (MHC) molecules, orchestration of leukocyte-endothelium interactions, effects on cell proliferation and apoptosis, as well as the stimulation and repression of a variety of genes whose functional significance remains obscure. The implementation of such a variety of effects by a single cytokine is achieved by complex patterns of cell-specific gene regulation: Several IFN-gamma-regulated genes are themselves components of transcription factors. The IFN-gamma response is itself regulated by interaction with responses to other cytokines including IFN-alpha/beta, TNF-alpha, and IL-4. Over 200 genes are now known to be regulated by IFN-gamma and they are listed in a World Wide Web document that accompanies this review. However, much of the cellular response to IFN-gamma can be described in terms of a set of integrated molecular programs underlying well-defined physiological systems, for example the induction of efficient antigen processing for MHC-mediated antigen presentation, which play clearly defined roles in pathogen resistance. A promising approach to the complexity of the IFN-gamma response is to extend the analysis of the less understood IFN-gamma-regulated genes in terms of molecular programs functional in pathogen resistance. more

Topics: Antigen presentation (60%), Antigen processing (59%), Major histocompatibility complex (58%) more

2,861 Citations

Journal ArticleDOI: 10.1126/SCIENCE.1087262
01 Aug 2003-Science
Abstract: Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense. more

Topics: TRIF (69%), Toll-like receptor (60%), TIRAP (58%) more

2,809 Citations

Journal ArticleDOI: 10.1098/RSPB.1957.0048
Alick Isaacs1, Jean Lindenmann1Institutions (1)
Abstract: During a study of the interference produced by heat-inactivated influenza virus with the growth of live virus in fragments of chick chorio-allantoic membrane it was found that following incubation of heated virus with membrane a new factor was released. This factor, recognized by its ability to induce interference in fresh pieces of chorio-allantoic membrane, was called interferon. Following a lag phase interferon was first detected in the membranes after 3 h incubation and thereafter it was released into the surrounding fluid. more

Topics: Viral Interference (57%), Virus (54%), Interferon (54%)

2,690 Citations

Journal ArticleDOI: 10.1126/SCIENCE.8009221
Ulrike Müller1, Ulrich Steinhoff1, Luiz F. L. Reis1, Silvio Hemmi1  +3 moreInstitutions (1)
24 Jun 1994-Science
Abstract: Mice lacking the known subunit of the type I interferon (IFN) receptor were completely unresponsive to type I IFNs, suggesting that this receptor chain is essential for type I IFN-mediated signal transduction. These mice showed no overt anomalies but were unable to cope with viral infections, despite otherwise normal immune responses. Comparison of mice lacking either type I or type II IFN receptors showed that, at least in response to some viruses, both IFN systems are essential for antiviral defense and are functionally nonredundant. more

Topics: Janus kinase 1 (64%), Interferon (53%), Immune system (51%) more

2,321 Citations

Open accessJournal ArticleDOI: 10.1126/SCIENCE.1232458
Lijun Sun1, Jiaxi Wu1, Fenghe Du1, Xiang Chen1  +1 moreInstitutions (1)
15 Feb 2013-Science
Abstract: The presence of DNA in the cytoplasm of mammalian cells is a danger signal that triggers host immune responses such as the production of type I interferons. Cytosolic DNA induces interferons through the production of cyclic guanosine monophosphate–adenosine monophosphate (cyclic GMP-AMP, or cGAMP), which binds to and activates the adaptor protein STING. Through biochemical fractionation and quantitative mass spectrometry, we identified a cGAMP synthase (cGAS), which belongs to the nucleotidyltransferase family. Overexpression of cGAS activated the transcription factor IRF3 and induced interferon-β in a STING-dependent manner. Knockdown of cGAS inhibited IRF3 activation and interferon-β induction by DNA transfection or DNA virus infection. cGAS bound to DNA in the cytoplasm and catalyzed cGAMP synthesis. These results indicate that cGAS is a cytosolic DNA sensor that induces interferons by producing the second messenger cGAMP. more

2,304 Citations

No. of papers in the topic in previous years

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Topic's top 5 most impactful authors

Thomas C. Merigan

110 papers, 6.7K citations

Adolfo García-Sastre

107 papers, 14.4K citations

Jan Vilcek

86 papers, 5.8K citations

Michael Gale

75 papers, 11.7K citations

Ion Gresser

58 papers, 5.2K citations

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