About this Research Topic
Cells of the immune system maintain homeostasis and gain pro-inflammatory functions to adapt to infection or other stressors. The NFkB pathway is a signal integration network that controls the expression of target genes involved in pro- and anti-inflammatory processes. Disruption of homeostasis, e.g. through exposure to pathogens or during wound healing, shifts the balance between the two outcomes. Deregulation of NFkB-dependent transcription is connected to life-threatening acute inflammation as well as many chronic diseases. Endogenously, the NFkB response is modulated by (i) complex, time-dependent negative feedback on upstream signaling nodes and (ii) gene-specific mechanisms such as transrepression. Pharmacological intervention at both levels is widely used in therapy exemplified by compounds that interfere with (i) proteasome-dependent degradation of negative regulators or (ii) expression of subsets of target genes.
Despite substantial efforts, the molecular mechanisms involved in the attenuation of NFkB-dependent transcription in hematopoietic cells have remained largely unclear, especially in gene-specific regulation. This Research Topic aims to elucidate molecular mechanisms that govern the balance between pro- and anti-inflammatory outputs in hematopoietic cells. At the level of cytoplasmic signaling, specific pharmacological control of the degradation of negative regulators of NFkB could improve current approaches to treat immunological disorders. General modulation of transrepression could fine-tune clinical tools. At both levels, more insight is needed to provide novel target structures. Moreover, the time-dependent signal integration by NFkB requires more delicate intervention than current options which largely ignore oscillatory mechanisms which are under-investigated.
In this Research Topic we welcome the submission of Original Research articles, Reviews, Mini-Reviews, Perspectives, and Hypothesis and Theory articles which cover, but are not limited to, the following topics:
• General mechanisms of transrepression (e.g. by nuclear receptor ligands)
• Modulation of NFkB signaling in monocytic cells
• Suppression of NFkB-dependent lymphoid cell functions
• Contributions of non-hematopoietic cells to immunomodulation via NFkB
Despite substantial efforts, the molecular mechanisms involved in the attenuation of NFkB-dependent transcription in hematopoietic cells have remained largely unclear, especially in gene-specific regulation. This Research Topic aims to elucidate molecular mechanisms that govern the balance between pro- and anti-inflammatory outputs in hematopoietic cells. At the level of cytoplasmic signaling, specific pharmacological control of the degradation of negative regulators of NFkB could improve current approaches to treat immunological disorders. General modulation of transrepression could fine-tune clinical tools. At both levels, more insight is needed to provide novel target structures. Moreover, the time-dependent signal integration by NFkB requires more delicate intervention than current options which largely ignore oscillatory mechanisms which are under-investigated.
In this Research Topic we welcome the submission of Original Research articles, Reviews, Mini-Reviews, Perspectives, and Hypothesis and Theory articles which cover, but are not limited to, the following topics:
• General mechanisms of transrepression (e.g. by nuclear receptor ligands)
• Modulation of NFkB signaling in monocytic cells
• Suppression of NFkB-dependent lymphoid cell functions
• Contributions of non-hematopoietic cells to immunomodulation via NFkB
Keywords: NFkB, immunomodulation, transrepression, hematopoietic cells
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