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10.3390/ijms22042177 http://scihub22266oqcxt.onion/10.3390/ijms22042177 33671651!7926921!33671651     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Sci 2021 ; 22 (4): ä Nephropedia Template TP {{tp|p=33671651|t=2021. sFasL-The Key to a Riddle: Immune Responses in Aging Lung and Disease |pdf=|usr=}}{{33671651}} gab.com Text sFasL-The Key to a Riddle: Immune Responses in Aging Lung and Disease JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33671651 #FOAvip By dint of the aging population and further deepened with the Covid-19 pandemic, lung disease has turned out to be a major cause of worldwide morbidity and mortality. The condition is exacerbated when the immune system further attacks the healthy, rather than the diseased, tissue within the lung. Governed by unremittingly proliferating mesenchymal cells and increased collagen deposition, if inflammation persists, as frequently occurs in aging lungs, the tissue develops tumors and/or turns into scars (fibrosis), with limited regenerative capacity and organ failure. Fas ligand (FasL, a ligand of the Fas cell death receptor) is a key factor in the regulation of these processes. FasL is primarily found in two forms: full length (membrane, or mFasL) and cleaved (soluble, or sFasL). We and others found that T-cells expressing the mFasL retain autoimmune surveillance that controls mesenchymal, as well as tumor cell accumulation following an inflammatory response. However, mesenchymal cells from fibrotic lungs, tumor cells, or cells from immune-privileged sites, resist FasL(+) T-cell-induced cell death. The mechanisms involved are a counterattack of immune cells by FasL, by releasing a soluble form of FasL that competes with the membrane version, and inhibits their cell death, promoting cell survival. This review focuses on understanding the previously unrecognized role of FasL, and in particular its soluble form, sFasL, in the serum of aged subjects, and its association with the evolution of lung disease, paving the way to new methods of diagnosis and treatment. Twit Text FOAVip sFasL-The Key to a Riddle: Immune Responses in Aging Lung and Disease ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33671651 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33671651 #FOAvip English Wikipedia <ref>{{Cite pmid|33671651}}</ref> sFasL-The Key to a Riddle: Immune Responses in Aging Lung and Disease #MMPMID33671651 Wallach-Dayan SB; Petukhov D; Ahdut-HaCohen R; Richter-Dayan M; Breuer R Int J Mol Sci 2021[Feb]; 22 (4): ä PMID33671651show ga By dint of the aging population and further deepened with the Covid-19 pandemic, lung disease has turned out to be a major cause of worldwide morbidity and mortality. The condition is exacerbated when the immune system further attacks the healthy, rather than the diseased, tissue within the lung. Governed by unremittingly proliferating mesenchymal cells and increased collagen deposition, if inflammation persists, as frequently occurs in aging lungs, the tissue develops tumors and/or turns into scars (fibrosis), with limited regenerative capacity and organ failure. Fas ligand (FasL, a ligand of the Fas cell death receptor) is a key factor in the regulation of these processes. FasL is primarily found in two forms: full length (membrane, or mFasL) and cleaved (soluble, or sFasL). We and others found that T-cells expressing the mFasL retain autoimmune surveillance that controls mesenchymal, as well as tumor cell accumulation following an inflammatory response. However, mesenchymal cells from fibrotic lungs, tumor cells, or cells from immune-privileged sites, resist FasL(+) T-cell-induced cell death. The mechanisms involved are a counterattack of immune cells by FasL, by releasing a soluble form of FasL that competes with the membrane version, and inhibits their cell death, promoting cell survival. This review focuses on understanding the previously unrecognized role of FasL, and in particular its soluble form, sFasL, in the serum of aged subjects, and its association with the evolution of lung disease, paving the way to new methods of diagnosis and treatment. |Age Factors[MESH] |Aged[MESH] |COVID-19/blood/*immunology[MESH] |Cell Death/immunology[MESH] |Fas Ligand Protein/blood/*immunology[MESH] |Humans[MESH] |Immunity[MESH] |Lung Diseases/blood/*immunology[MESH] |Lung/*immunology[MESH] |SARS-CoV-2/immunology/isolation & purification[MESH]sFasL-The Key to a Riddle: Immune Responses in Aging Lung and Disease (epmc).pdf DeepDyve Pubget Overpricing