1,721,041 research outputs found
Editorial: Regulation of Soluble Immune Mediators by Non-Coding RNAs
Full text linkNon-coding RNAs (ncRNAs), defined as transcripts that do not encode proteins, are known since long time for their role in translation (i.e. transfer RNAs, ribosomal RNAs) and in splicing events (i.e. small nuclear and small nucleolar RNAs). However, only recently, the revolutionary advances in deep sequencing technology brought to light several new classes of ncRNA, classified according to their length into “short” ncRNAs (<200 nucleotides, that includes piwi-associated RNAs, endogenous short-interfering RNAs, microRNAs, Y-RNAs and others), and “long” ncRNAs (lncRNAs, >200 nucleotides) (1). Cytokines are crucial soluble messengers of the immune system that regulate and sustain inflammation and immunity. Cytokine expression is tightly regulated, reflecting the need of the immune system to tailor the magnitude and duration of its responses to induce pathogen clearance, but not tissue damage. Thus, understanding cytokine regulation is crucial to gain insight and eventually manipulate undesired immune responses. In this Research Topic, 53 authors contributed 11 articles touching on many of the combined roles of ncRNAs on the production of cytokines and their consequential effect on cytokine-related functional outputs, as well as inflammatory/autoimmune pathologies
Interactions of NF-kappaB with chromatin: the art of being at the right place at the right time.
No full textTranscription factors of the NF-kappaB family are essential regulators of the inflammatory and immune responses. The main 'switch' in NF-kappaB activation is cytoplasmic and leads to the release of NF-kappaB proteins from IkappaB molecules, specific inhibitors that prevent their nuclear accumulation. However, it is becoming increasingly apparent that in addition to this required activation step, both recruitment of NF-kappaB to target genes and NF-kappaB-induced transcriptional events after recruitment are actively controlled. Regulated recruitment of NF-kappaB to chromatin generates kinetic complexity in NF-kappaB-dependent gene induction and 'wires' NF-kappaB-regulated gene activity to simultaneously activated pathways and transcription factors
The toll-like repertoire of human B lymphocytes: inducible and selective expression of TLR9 and TLR10 in normal and transformed cells.
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Plastic downregulation of the transcriptional repressor BCL6 during maturation of human dendritic cells.
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Immune functions and recruitment of plasmacytoid dendritic cells in psoriasis.
No full textPsoriasis is one of the most common chronic T cell-mediated diseases in humans. Among the most proximal event in the innate immunity cascade driving psoriatic inflammation is the secretion of type I IFN by activated plasmacytoid dendritic cells (pDC), a special DC subset strategically positioned in pre-psoriatic symptomless skin. There is an IFN-alpha signature in primary psoriatic plaques, and blocking of type I IFN signalling can prevent the expansion of pathogenetic T cells and development of psoriatic phenotype. Recently, we have demonstrated that pDC infiltration in psoriatic skin correlates with the expression of markers typical of early phases of psoriasis, whereas it is almost absent in long-lasting lesions. Importantly, pDC recruitment in psoriatic skin is strictly associated with the chemerin/ChemR23 axis, and is temporally active during psoriatic plaque development. Pro-chemerin is produced primarily by dermal fibroblasts, but also by mast cells and endothelial cells. Once secreted, it can be activated by enzymes produced by neutrophils and mast cells, which infiltrate early psoriasis lesions. These findings propose the chemerin/ChemR23 axis as a potential novel therapeutic target in psoriasis
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