Type I Interferons

Maeyer, Edward De; Maeyer‐Guignard, Jaqueline De

doi:10.3109/08830189809084487

Cited by 103 publications

(60 citation statements)

References 109 publications

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“…The IFNAR-2 is the subunit responsible for the interaction with the ligand. There are three forms of IFNAR-2, which are differentially spliced products of the same gene, e.g., the soluble (IFNAR-2a), short (IFNAR-2b), and long (IFNAR-2c) forms (26,31,32). The chain IFNAR-2c with its long cytoplasmic domain and the IFNAR-1 subunit constitute the predominantly active form of the type I IFN receptor complex.…”

Section: Discussionmentioning

confidence: 99%

“…IFN-a is currently used as a therapeutic agent in several malignancies, including GEP-NETs (14)(15)(16)(26)(27)(28)(29). This cytokine belongs to the class of type I IFNs (e.g., IFN-a, IFN-h, IFN-N, IFNn, and IFN-H ), which modulate a variety of biological responses through the activation of a common receptor, composed by two subunits: IFNAR-1 and IFNAR-2 (30,31).…”

Section: Discussionmentioning

confidence: 99%

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IFN-β Is a Highly Potent Inhibitor of Gastroenteropancreatic Neuroendocrine Tumor Cell Growth In vitro

et al. 2006

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IFN-A controls hormone secretion and symptoms in human gastroenteropancreatic neuroendocrine tumors (GEP-NET) but it rarely induces a measurable tumor size reduction. The effect of other type I IFNs, e.g., IFN-B, has not been evaluated. We compared the antitumor effects of IFN-A and IFN-B in BON cells, a functioning human GEP-NET cell line. As determined by quantitative reverse transcription-PCR analysis and immunocytochemistry, BON cells expressed the active type I IFN receptor mRNA and protein (IFNAR-1 and IFNAR-2c subunits). After 3 and 6 days of treatment, IFN-B significantly inhibited BON cell growth in a time-and dose-dependent manner. IC 50 and maximal inhibitory effect on day 6 were 8 IU/mL and 98%, respectively. In contrast, the effect of IFN-A resulted significantly in a less potent effect (IC 50 : 44 IU/mL, maximal inhibition: 26%). IFN-A induced only cell cycle arrest, with an accumulation of the cells in S phase. IFN-B, apart from a more potent delay in S-G 2 -M phase transit of the cell cycle, also induced a strong stimulation of apoptosis, evaluated by flow cytometry (Annexin V and 7-AAD) and measurement of the DNA fragmentation. Besides, only IFN-B severely suppressed chromogranin A levels in the medium from BON cells after 6 days of treatment. In conclusion, IFN-B is much more potent, compared with IFN-A, in its inhibitory effect on GEP-NET cell proliferation in vitro through the induction of apoptosis and cell cycle arrest. Further studies are required to establish whether IFN-B has comparable potent tumor growth inhibitory effects in vivo. (Cancer Res 2006; 66(1): 554-62)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

IFN-β Is a Highly Potent Inhibitor of Gastroenteropancreatic Neuroendocrine Tumor Cell Growth In vitro

et al. 2006

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“…Type I IFN plays a critical role in initiating antiviral innate immunity and modulating subsequent adaptive immunity (1,2). A dsRNA-induced signal is transmitted to the nucleus via a series of transcription factors, including IFN regulatory factor (IRF) 3 -3, IRF-7, NF-B, and activating transcription factor-2/c-Jun (3).…”

mentioning

confidence: 99%

Shared and Unique Functions of the DExD/H-Box Helicases RIG-I, MDA5, and LGP2 in Antiviral Innate Immunity

Yoneyama

Kikuchi

Matsumoto

et al. 2005

The Journal of Immunology

1,464

1,296

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The cellular protein retinoic acid-inducible gene I (RIG-I) senses intracellular viral infection and triggers a signal for innate antiviral responses including the production of type I IFN. RIG-I contains a domain that belongs to a DExD/H-box helicase family and exhibits an N-terminal caspase recruitment domain (CARD) homology. There are three genes encoding RIG-I-related proteins in human and mouse genomes. Melanoma differentiation associated gene 5 (MDA5), which consists of CARD and a helicase domain, functions as a positive regulator, similarly to RIG-I. Both proteins sense viral RNA with a helicase domain and transmit a signal downstream by CARD; thus, these proteins share overlapping functions. Another protein, LGP2, lacks the CARD homology and functions as a negative regulator by interfering with the recognition of viral RNA by RIG-I and MDA5. The nonstructural protein 3/4A protein of hepatitis C virus blocks the signaling by RIG-I and MDA5; however, the V protein of the Sendai virus selectively abrogates the MDA5 function. These results highlight ingenious mechanisms for initiating antiviral innate immune responses and the action of virus-encoded inhibitors.

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“…Type I IFNs (IFN-I) were discovered on the basis of their antiviral activity and comprise a conserved family of pleiotropic cytokines that are produced by a variety of cells, including fibroblasts, macrophages, and dendritic cells (14,15). They are critical to the host antiviral defense and are important to the innate and adaptive immunity to several microorganisms because they activate macrophages and NK cells and costimulate T cell proliferation and differentiation (16 -18).…”

mentioning

confidence: 99%

Type I IFNs Stimulate Nitric Oxide Production and Resistance to Trypanosoma cruzi Infection

Costa

Torres

Mendonça

et al. 2006

The Journal of Immunology

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The participation of type I IFNs (IFN-I) in NO production and resistance to Trypanosoma cruzi infection was investigated. Adherent cells obtained from the peritoneal cavity of mice infected by the i.p. route produced NO and IFN-I. Synthesis of NO by these cells was partially inhibited by treatment with anti-IFN-αβ or anti-TNF-α Abs. Compared with susceptible BALB/c mice, peritoneal cells from parasite-infected resistant C57BL/6 mice produced more NO (2-fold), IFN-I (10-fold), and TNF-α (3.5-fold). Later in the infection, IFN-I levels measured in spleen cell (SC) cultures from 8-day infected mice were greater in C57BL/6 than in infected BALB/c mice, and treatment of the cultures with anti-IFN-αβ Ab reduced NO production. IFN-γ or IL-10 production by SCs was not different between the two mouse strains; IL-4 was not detectable. Treatment of C57BL/6 mice with IFN-I reduced parasitemia levels in the acute phase of infection. Mice deprived of the IFN-αβR gene developed 3-fold higher parasitemia levels in the acute phase in comparison with control 129Sv mice. Production of NO by peritoneal macrophages and SCs was reduced in mice that lacked signaling by IFN-αβ, whereas parasitism of macrophages was heavier than in control wild-type mice. We conclude that IFN-I costimulate NO synthesis early in T. cruzi infection, which contributes to a better control of the parasitemia in resistant mice.

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Type I Interferons

Cited by 103 publications

References 109 publications

IFN-β Is a Highly Potent Inhibitor of Gastroenteropancreatic Neuroendocrine Tumor Cell Growth In vitro

IFN-β Is a Highly Potent Inhibitor of Gastroenteropancreatic Neuroendocrine Tumor Cell Growth In vitro

Shared and Unique Functions of the DExD/H-Box Helicases RIG-I, MDA5, and LGP2 in Antiviral Innate Immunity

Type I IFNs Stimulate Nitric Oxide Production and Resistance to Trypanosoma cruzi Infection

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