Modulation of Pro-Inflammatory Signaling by Interferons

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About this Research Topic

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Background

Interferons are crucial regulators of the immune response, and both pro- and anti-inflammatory effects have been described for these cytokines. While their classical function is anti-viral activity and the defense against diverse forms of microbial infections, interferons are also involved in anti-tumor immunity, autoimmunity, cell development, homeostasis, tissue protection, and metabolism. Three types of interferons are known, with IFN-α, -β (type I), and -γ (type II) as the most prominent representatives. Following stimulation with interferons, intracellular signaling pathways are initiated (classically the Jak-STAT pathway), interferon-stimulated genes are activated (including epigenomic remodeling), and subsequent cellular processes - such as antiviral programs - are executed. However, due to the variety of potentially activated signaling cascades, shared target gene promoter elements, and the specific characteristics of interferon-responsive cells (among other things), different (types of) interferons may have distinct as well as overlapping functions.

Under both physiological and pathophysiological conditions, however, interferons do not act on their target cells alone, but are part of a complex cocktail of different cytokines/chemokines, growth factors, anti-microbial peptides, soluble adhesion molecules, lipid mediators, etc., whose interaction defines the reaction of the cells to the specific stimulatory situation. The presence of interferons may significantly modulate the impact of these factors (and vice versa), resulting in either synergistic or antagonistic effects on the activation of pro-inflammatory signaling pathways and the magnitude of the respective response. Alterations in the controlled progress of the inflammatory response may lead to severe dysregulations and to infectious, inflammatory, metabolic, or malignant diseases. Thus, this article collection aims at further elucidating the molecular events adjusting the outcome of cellular stimulation by different pro- or anti-inflammatory mediators in cooperation or competition with interferons.

This Research Topic will focus on the diverse molecular mechanisms by which interferons affect, modify, and control pro-inflammatory signaling cascades at multiple levels as well as the consequences - either beneficial or detrimental - of this modulation for immunity and homeostasis. All types of articles (including Original and Review Articles, Brief Reports, Perspectives, Hypotheses, Opinions, and Clinical Trials) are welcome. The following subtopics will be predominantly (but not exclusively) included:

- Distinct and overlapping functions of different types of interferons.
- Regulation of signaling pathways by interferons and pro- or anti-inflammatory cytokines.
- Crosstalk of interferons and other mediators in the regulation of epigenetic, transcriptional, and post-transcriptional processes.
- Modulation of interferon-stimulated gene expression patterns by other mediators (and vice versa).
- Modulation of LPS- and TNF-tolerance by interferons.
- Pharmacological intervention in interferon-dependent signaling.
- Influence of interferon-containing cytokine cocktails on cell shape and development.
- Interferon-associated (auto-)inflammatory disorders and interferonopathies.
- Co-operation of interferons and further cytokines in infectious, inflammatory, metabolic, and malignant diseases.

Keywords: interferons, cytokines, mutual regulation, modulation of pro-inflammatory signaling, interferon-stimulated genes, inflammation, autoimmunity, interferon-associated diseases

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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