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Pharmaceuticals
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Interferons 2015
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Interferons 2015

A special issue of Pharmaceuticals (ISSN 1424-8247).

Deadline for manuscript submissions: closed (30 June 2015)

Special Issue Editor

Dr. Howard A. Young

E-Mail Website
Guest Editor
Principal Investigator & Deputy Lab Chief, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Bldg. 560/31-23, Chandler Street, Frederick, MD 21702-1201, USA
Interests: interferon-gamma; cytokines, interferons, post transcriptional mRNA regulation; interleukins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues

The journal Pharmaceuticals will be publishing a Special Issue covering the topic, “Interferons”, and I cordially invite you to contribute an article to this volume.

Since their discovery over 50 years ago, interferons have impacted cancer research, autoimmunity, and host responses to infection. Also, a huge commercial market has developed for interferons because they became critical for treating hepatitis B and C. However, the use of interferons is changing. This Special Issue will highlight recent developments in the clinical use of these drugs (including Type I, II, and III interferons). In addition, we welcome the presentation and discussion of new preclinical models for interferons in order to offer participants a vision into the future of interferons in the clinic.

Dr. Howard A. Young
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


Keywords

  • interferon
  • interleukins
  • pre-clinical models
  • clinical applications
  • STAT
  • receptors
  • gene induction
  • cancer
  • autoimmunity
  • infectious diseases

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Published Papers (3 papers)

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Research

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299 KiB  
Article
Tryptophan Breakdown in Patients with HCV Infection is Influenced by IL28B Polymorphism
by Heinz Zoller, Annina Jenal, Albert F. Staettermayer, Sebastian Schroecksnadel, Peter Ferenci and Dietmar Fuchs
Pharmaceuticals 2015, 8(2), 337-350; https://doi.org/10.3390/ph8020337 - 18 Jun 2015
Cited by 6 | Viewed by 5652
Abstract
Until recently, the standard treatment of chronic hepatitis C virus (HCV) infection was a combination therapy with PEG-IFN-α plus ribavirin. Previous studies have proven that several markers predict the outcome of such therapy, e.g., pretreatment plasma levels of interferon inducible protein IP-10, HCV [...] Read more.
Until recently, the standard treatment of chronic hepatitis C virus (HCV) infection was a combination therapy with PEG-IFN-α plus ribavirin. Previous studies have proven that several markers predict the outcome of such therapy, e.g., pretreatment plasma levels of interferon inducible protein IP-10, HCV RNA and IL28B-related single nucleotide polymorphisms (SNP). Altered activity of tryptophan metabolizing enzyme indoleamine 2,3-dioxygenase (IDO) has been also shown in patients suffering from HCV infection. In this study, we investigated whether IL28B SNP in patients infected with HCV is related to the tryptophan breakdown rate. Before therapy, serum tryptophan and kynurenine concentrations were determined in 25 patients with established HCV infection and the kynurenine to tryptophan ratio (KYN/TRP) was calculated as an estimate of the tryptophan breakdown rate. In parallel, neopterin and nitrite concentrations were determined. A significant difference of serum KYN/TRP existed between the three IL28B polymorphism groups: C/C genotype had the highest and T/T genotype had the lowest KYN/TRP (p < 0.05). Likewise, C/C genotype was associated with higher KYN/TRP than non-C/C genotype (p = 0.01). There was a smaller difference between the three groups regarding the absolute kynurenine concentrations, the C/C genotype being associated with higher kynurenine concentrations. None of the other comparisons revealed any statistical significance. In conclusion, patients with C/C genotype presented with the highest tryptophan breakdown rate already before antiretroviral therapy with IFN-α/ribavirin. The differences in tryptophan metabolism might relate to HCV clearance and also to side effects of IFN-α therapy. Full article
(This article belongs to the Special Issue Interferons 2015)
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Review

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794 KiB  
Review
The Type I IFN-Induced miRNA, miR-21
by Chuan He Yang, Kui Li, Susan R. Pfeffer and Lawrence M. Pfeffer
Pharmaceuticals 2015, 8(4), 836-847; https://doi.org/10.3390/ph8040836 - 25 Nov 2015
Cited by 25 | Viewed by 5264
Abstract
The interferon (IFN) family of cytokines not only has antiviral properties at various steps in the viral replication cycle, but also anticancer activity through multiple pathways that include inhibiting cell proliferation, regulating cellular responses to inducers of apoptosis and modulating angiogenesis and the [...] Read more.
The interferon (IFN) family of cytokines not only has antiviral properties at various steps in the viral replication cycle, but also anticancer activity through multiple pathways that include inhibiting cell proliferation, regulating cellular responses to inducers of apoptosis and modulating angiogenesis and the immune system. IFNs are known to induce their biological activity through the induction of protein encoding IFN-stimulated genes. However, recent studies have established that IFNs also induce the expression of microRNAs (miRNAs), which are small endogenous non-coding RNAs that suppress gene expression at the post-transcriptional level. MiRNAs play critical roles in tumorigenesis and have been implicated to act as either oncogenes or tumor suppressors in various human cancers. Therefore, IFN-induced miRNAs play an important role, not only in the host response to innate immune response to cancer, but also in the tumorigenic process itself. Furthermore, IFN-induced miRNAs may participate in and/or orchestrate antiviral defense in certain viral infections. In this review, we describe our recent studies on the induction of miR-21 by type I IFN, the role of the STAT3 and NFκB signaling pathways in IFN-induced miR-21 expression, the role of miR-21 in different cancers and the role of miR-21 in regulating the antiviral response. Full article
(This article belongs to the Special Issue Interferons 2015)
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749 KiB  
Review
Therapeutic Potential of Interferon-γ and Its Antagonists in Autoinflammation: Lessons from Murine Models of Systemic Juvenile Idiopathic Arthritis and Macrophage Activation Syndrome
by Anneleen Avau and Patrick Matthys
Pharmaceuticals 2015, 8(4), 793-815; https://doi.org/10.3390/ph8040793 - 25 Nov 2015
Cited by 16 | Viewed by 7242
Abstract
Interferon-γ (IFN-γ) affects immune responses in a complex fashion. Its immunostimulatory actions, such as macrophage activation and induction of T helper 1-type responsiveness, are widely acknowledged, however, as documented by a large body of literature, IFN-γ has also the potential to temper inflammatory [...] Read more.
Interferon-γ (IFN-γ) affects immune responses in a complex fashion. Its immunostimulatory actions, such as macrophage activation and induction of T helper 1-type responsiveness, are widely acknowledged, however, as documented by a large body of literature, IFN-γ has also the potential to temper inflammatory processes via other pathways. In autoimmune and autoinflammatory disorders, IFN-γ can either play a disease-enforcing role or act as protective agent, depending on the nature of the disease. In animal models of any particular autoimmune disease, certain changes in the induction procedure can reverse the net outcome of introduction or ablation of IFN-γ. Here, we review the role of endogenous IFN-γ in inflammatory disorders and related murine models, with a focus on systemic juvenile idiopathic arthritis (sJIA) and macrophage activation syndrome (MAS). In particular, we discuss our recent findings in a mouse model of sJIA, in which endogenous IFN-γ acts as a regulatory agent, and compare with results from mouse models of MAS. Also, we elaborate on the complexity in the activity of IFN-γ and the resulting difficulty of predicting its value or that of its antagonists as treatment option. Full article
(This article belongs to the Special Issue Interferons 2015)
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