Following an acute inflammatory response, its well-controlled resolution is required to restore homeostasis. A dysregulation in this crucial phase may result in chronic inflammation and contribute to the development of autoimmune diseases. Resolution of inflammation may involve a variety of different, but mutually supportive cellular and intracellular events. For instance, the differential recruitment and (in)activation of different subsets of immune cells, apoptosis, clearance of apoptotic cells, and tissue repair processes are of importance. Moreover, the controlled expression/secretion of pro-resolving lipid mediators and pro-/anti-inflammatory cytokines, metabolic shifts, and the termination of activated pro-inflammatory signaling pathways are key events in this context.
The exposure of cells to pro-inflammatory mediators may result in an intense activation of intracellular signaling pathways. In consequence, the termination of pro-inflammatory mediator-induced signaling is an essential step in the controlled attenuation of inflammation, which can occur at multiple levels along the signaling cascade up to (post-) transcriptional processes. In autoimmune diseases, however, a variety of aberrations may emerge at these regulatory steps. Despite several groundbreaking studies, the detailed mechanisms influencing the termination of signal transduction and the respective disturbances playing a role in the development and perpetuation of autoimmune diseases are insufficiently described. Thus, the aim of this article collection is to further elucidate the intracellular machinery that terminates inflammation-promoting and -sustaining signaling events and to gain new insights in the divers mis-regulations contributing to autoimmunity.
This article collection focuses on the molecular mechanisms involved in the restriction/suppression of pro-inflammatory signal transduction and the various dysregulations occurring in autoimmune diseases. All types of articles (including Original Research and Review articles, Perspectives, Hypothesis and Theory, Opinions, and Clinical Trials) are welcome. In detail, the following subtopics will be predominantly (but not exclusively) included:
- Abundance of relevant functional receptors on the cell surface
- (Omitted) suppression of signal transduction initiation by receptor-associated protein complexes
- (Dysregulated) activity of kinases, phosphatases, proteases, and other regulatory entities involved in the inactivation of pro-inflammatory signaling pathways
- (Disturbances in) transcriptional and post-transcriptional processes, e.g., regulating the expression of pro- and anti-inflammatory mediators
- Pharmacological modulation of signal transduction to restrict excessive inflammation
Following an acute inflammatory response, its well-controlled resolution is required to restore homeostasis. A dysregulation in this crucial phase may result in chronic inflammation and contribute to the development of autoimmune diseases. Resolution of inflammation may involve a variety of different, but mutually supportive cellular and intracellular events. For instance, the differential recruitment and (in)activation of different subsets of immune cells, apoptosis, clearance of apoptotic cells, and tissue repair processes are of importance. Moreover, the controlled expression/secretion of pro-resolving lipid mediators and pro-/anti-inflammatory cytokines, metabolic shifts, and the termination of activated pro-inflammatory signaling pathways are key events in this context.
The exposure of cells to pro-inflammatory mediators may result in an intense activation of intracellular signaling pathways. In consequence, the termination of pro-inflammatory mediator-induced signaling is an essential step in the controlled attenuation of inflammation, which can occur at multiple levels along the signaling cascade up to (post-) transcriptional processes. In autoimmune diseases, however, a variety of aberrations may emerge at these regulatory steps. Despite several groundbreaking studies, the detailed mechanisms influencing the termination of signal transduction and the respective disturbances playing a role in the development and perpetuation of autoimmune diseases are insufficiently described. Thus, the aim of this article collection is to further elucidate the intracellular machinery that terminates inflammation-promoting and -sustaining signaling events and to gain new insights in the divers mis-regulations contributing to autoimmunity.
This article collection focuses on the molecular mechanisms involved in the restriction/suppression of pro-inflammatory signal transduction and the various dysregulations occurring in autoimmune diseases. All types of articles (including Original Research and Review articles, Perspectives, Hypothesis and Theory, Opinions, and Clinical Trials) are welcome. In detail, the following subtopics will be predominantly (but not exclusively) included:
- Abundance of relevant functional receptors on the cell surface
- (Omitted) suppression of signal transduction initiation by receptor-associated protein complexes
- (Dysregulated) activity of kinases, phosphatases, proteases, and other regulatory entities involved in the inactivation of pro-inflammatory signaling pathways
- (Disturbances in) transcriptional and post-transcriptional processes, e.g., regulating the expression of pro- and anti-inflammatory mediators
- Pharmacological modulation of signal transduction to restrict excessive inflammation
