Cytokine JAK-STAT Signaling in Immunity

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

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