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10.3389/fimmu.2017.00345 http://scihub22266oqcxt.onion/10.3389/fimmu.2017.00345 C5378711!5378711!28421072     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28421072|t=2017. Dysregulated IL-1? Secretion in Autoinflammatory Diseases: A Matter of Stress?|pdf=|usr=}}{{28421072}} gab.com Text Dysregulated IL-1 Secretion in Autoinflammatory Diseases: A Matter of Stress JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28421072 #FOAvip Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1?. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1? production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation. Twit Text FOAVip Dysregulated IL-1 Secretion in Autoinflammatory Diseases: A Matter of Stress ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28421072 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28421072 #FOAvip English Wikipedia <ref>{{Cite pmid|28421072}}</ref> Dysregulated IL-1? Secretion in Autoinflammatory Diseases: A Matter of Stress? #MMPMID28421072 Carta S; Semino C; Sitia R; Rubartelli A Front Immunol 2017[]; 8 (ä): ä PMID28421072show ga Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1?. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1? production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation. äDysregulated IL-1? Secretion in Autoinflammatory Diseases: A Matter of(epmc).pdf DeepDyve Pubget Overpricing