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Vaccines
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Cytokine JAK-STAT Signaling in Immunity
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Cytokine JAK-STAT Signaling in Immunity

A special issue of Vaccines (ISSN 2076-393X).

Deadline for manuscript submissions: closed (31 October 2016) | Viewed by 38225

Special Issue Editor

Prof. Mirko Trilling

E-Mail Website
Guest Editor
Institute for Virology, University Hospital Essen, University Duisburg-Essen, Essen D-45147, Germany
Interests: Herpesviruses; JAK-STAT signaling; interferon; interferon antagonists; immune evasion; ubiquitin/proteasome system

Special Issue Information

Dear Colleagues,

Immune responses represent highly concerted and coordinated processes for which cellular communication is absolutely indispensable. Main mediators of the respective signaling network are cytokines. Consistently, an understanding of expression profiles and functional activities of cytokines and their cognate receptors has become a fundamental aspect of current immunology.

A multiplicity of cytokines (e.g., interferons and interleukin [IL]-2, -4, -6, -10 & -12) with key roles in immunity exert their biological activity primarily via alteration of transcriptional profiles induced by signal transducer and activators of transcription (STAT). STATs become activated upon tyrosine phosphorylation catalysed by receptor-associated Janus kinases (JAK). Signal transduction via JAKs and STATs is very rapid due to the fact that STATs are usually pre-existent and can be immediately activated.

The importance of cytokine-induced JAK-STAT signaling for immunity is highlighted by drastically increased pathogen susceptibility of individuals with detrimental mutations and mice with targeted deletions affecting genes encoding components of these pathways. Moreover, pathogen-encoded virulence factors which antagonize cytokine signalling underline the pivotal role of cellular communication for immune control.

This special issue of Vaccines will focus on the role of cytokine-induced JAK-STAT signaling in the context of innate and adaptive immune responses.
This special issue covers all the following potential topics, but not limited:

  • Nuclear translocation and cycling of STATs
  • Serine phosphorylation of STATs
  • Cross-talk between JAK-STAT pathways
  • Receptor scaffolding and sorting functions of Janus kinases
  • Mouse models as approach to study the biological relevance of JAKs and STATs
  • Unanticipated lessons from human JAK-STAT mutations
  • Nuclear roles of JAKs?
  • The role of pre-existing STAT dimers for signaling
  • How can cytokines with apparently opposing biological functions signal via the same STATs?
  • Connections between JAK-STAT and TNF-NF-κB signaling
  • STAT3: Pro-inflammatory, anti-inflammatory or both?
  • STATs and CD4 differentiation
  • Pathogen-encoded antagonists targeting JAK-STAT signaling
  • Pathogen-encoded exploitation of JAK-STAT signaling

Professor Dr. Mirko Trilling
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. Vaccines 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 2700 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
  • Janus kinases (JAK)
  • Signal transducer and activator of transcription (STAT)
  • Cytokines
  • Innate immunity
  • Adaptive immunity

Published Papers (3 papers)

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Review

1667 KiB  
Review
Leptin-Induced JAK/STAT Signaling and Cancer Growth
by McKay Mullen and Ruben Rene Gonzalez-Perez
Vaccines 2016, 4(3), 26; https://doi.org/10.3390/vaccines4030026 - 26 Jul 2016
Cited by 110 | Viewed by 10000
Abstract
Growth factor and cytokine signaling can influence the development of several cancer types. One of the key players in the development of cancer is the Janus kinas (JAK) signal transducer of activators of transcription (STAT) signaling pathway. The majority of growth factors and [...] Read more.
Growth factor and cytokine signaling can influence the development of several cancer types. One of the key players in the development of cancer is the Janus kinas (JAK) signal transducer of activators of transcription (STAT) signaling pathway. The majority of growth factors and cytokine interactions with their membrane-bound receptors trigger JAK-STAT activation. The influential relationship between obesity and cancer is a fact. However, there is a complex sequence of events contributing to the regulation of this mechanism to promote tumor growth, yet to be fully elucidated. The JAK-STAT pathway is influenced by obesity-associated changes that have been shown to impact cancer growth and progression. This intricate process is highly regulated by a vast array of adipokines and cytokines that exert their pleiotropic effects on cancer cells to enhance metastasis to distant target sites. Leptin is a cytokine, or more precise, an adipokine secreted mainly by adipose tissue that requires JAK-STAT activation to exert its biological functions. Leptin is the central regulator of energy balance and appetite. Leptin binding to its receptor OB-R in turn activates JAK-STAT, which induces proliferation, angiogenesis, and anti-apoptotic events in normal cells and malignant cells expressing the receptor. Leptin also induces crosstalk with Notch and IL-1 (NILCO), which involves other angiogenic factors promoting tumor growth. Therefore, the existence of multiple novel classes of therapeutics that target the JAK/STAT pathway has significant clinical implications. Then, the identification of the signaling networks and factors that regulate the obesity-cancer link to which potential pharmacologic interventions can be implemented to inhibit tumor growth and metastasis. In this review, we will discuss the specific relationship between leptin-JAK-STAT signaling and cancer. Full article
(This article belongs to the Special Issue Cytokine JAK-STAT Signaling in Immunity)
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Graphical abstract

568 KiB  
Review
Viral Inhibition of the IFN-Induced JAK/STAT Signalling Pathway: Development of Live Attenuated Vaccines by Mutation of Viral-Encoded IFN-Antagonists
by Stephen B. Fleming
Vaccines 2016, 4(3), 23; https://doi.org/10.3390/vaccines4030023 - 29 Jun 2016
Cited by 89 | Viewed by 15584
Abstract
The interferon (IFN) induced anti-viral response is amongst the earliest and most potent of the innate responses to fight viral infection. The induction of the Janus kinase/signal transducer and activation of transcription (JAK/STAT) signalling pathway by IFNs leads to the upregulation of hundreds [...] Read more.
The interferon (IFN) induced anti-viral response is amongst the earliest and most potent of the innate responses to fight viral infection. The induction of the Janus kinase/signal transducer and activation of transcription (JAK/STAT) signalling pathway by IFNs leads to the upregulation of hundreds of interferon stimulated genes (ISGs) for which, many have the ability to rapidly kill viruses within infected cells. During the long course of evolution, viruses have evolved an extraordinary range of strategies to counteract the host immune responses in particular by targeting the JAK/STAT signalling pathway. Understanding how the IFN system is inhibited has provided critical insights into viral virulence and pathogenesis. Moreover, identification of factors encoded by viruses that modulate the JAK/STAT pathway has opened up opportunities to create new anti-viral drugs and rationally attenuated new generation vaccines, particularly for RNA viruses, by reverse genetics. Full article
(This article belongs to the Special Issue Cytokine JAK-STAT Signaling in Immunity)
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1516 KiB  
Review
Integrating Immunologic Signaling Networks: The JAK/STAT Pathway in Colitis and Colitis-Associated Cancer
by Sebastian Zundler and Markus F. Neurath
Vaccines 2016, 4(1), 5; https://doi.org/10.3390/vaccines4010005 - 29 Feb 2016
Cited by 76 | Viewed by 12028
Abstract
Cytokines are believed to be crucial mediators of chronic intestinal inflammation in inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) and ulcerative colitis (UC). Many of these cytokines trigger cellular effects and functions through signaling via janus kinase (JAK) and signal transducer [...] Read more.
Cytokines are believed to be crucial mediators of chronic intestinal inflammation in inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) and ulcerative colitis (UC). Many of these cytokines trigger cellular effects and functions through signaling via janus kinase (JAK) and signal transducer and activator of transcription (STAT) molecules. In this way, JAK/STAT signaling controls important events like cell differentiation, secretion of cytokines or proliferation and apoptosis in IBD in both adaptive and innate immune cells. Moreover, JAK/STAT signaling, especially via the IL-6/STAT3 axis, is believed to be involved in the transition of inflammatory lesions to tumors leading to colitis-associated cancer (CAC). In this review, we will introduce the main cellular players and cytokines that contribute to pathogenesis of IBD by JAK/STAT signaling, and will highlight the integrative function that JAK/STATs exert in this context as well as their divergent role in different cells and processes. Moreover, we will explain current concepts of the implication of JAK/STAT signaling in CAC and finally discuss present and future therapies for IBD that interfere with JAK/STAT signaling. Full article
(This article belongs to the Special Issue Cytokine JAK-STAT Signaling in Immunity)
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