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10.1038/cddis.2017.144 http://scihub22266oqcxt.onion/10.1038/cddis.2017.144 C5386542!5386542!28358370     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (3): e2721- Nephropedia Template TP {{tp|p=28358370|t=2017. The role of autophagy in asparaginase-induced immune suppression of macrophages |pdf=|usr=}}{{28358370}} gab.com Text The role of autophagy in asparaginase-induced immune suppression of macrophages JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28358370 #FOAvip Erwinia asparaginase, a bacteria-derived enzyme drug, has been used in the treatment of various cancers, especially acute lymphoblastic leukemia (ALL). One of the most significant side effects associated with asparaginase administration is immune suppression, which limits its application in clinic. Macrophages are phagocytic immune cells and have a central role in inflammation and host defense. We reported here that asparaginase disturbed the function of macrophages including phagocytosis, proliferation, ROS and nitric oxide secretion, interleukin 6 (IL-6) and tumor necrosis factor ? (TNF-?) secretion, and major histocompatibility complex II (MHC-II) molecule expression, thus induced immune suppression in interferon-? and lipopolysaccharide-stimulated macrophages. We also observed that asparaginase inhibited autophagy in macrophages via activating Akt/mTOR and suppressing Erk1/2 signaling pathway as evidenced by less formation of autophagosomes, downregulation of autophagy-related protein LC3-II, and decreased number of autophagy-like vacuoles. Further study discovered that treatment with autophagy inhibitor 3-MA in place of asparaginase on activated macrophages could also downregulate phagocytosis, cytokine secretion, and MHC-II expression. Moreover, incubation with autophagy inducer trehalose restored the capacity of phagocytosis, IL-6 and TNF-? secretion, and MHC-II expression in macrophages. These results prove the important role of autophagy in the function of macrophages, and activation of autophagy can overcome asparaginase-induced immune suppression in macrophages. Twit Text FOAVip The role of autophagy in asparaginase-induced immune suppression of macrophages ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28358370 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28358370 #FOAvip English Wikipedia <ref>{{Cite pmid|28358370}}</ref> The role of autophagy in asparaginase-induced immune suppression of macrophages #MMPMID28358370 Song P; Wang Z; Zhang X; Fan J; Li Y; Chen Q; Wang S; Liu P; Luan J; Ye L; Ju D Cell Death Dis 2017[Mar]; 8 (3): e2721- PMID28358370show ga Erwinia asparaginase, a bacteria-derived enzyme drug, has been used in the treatment of various cancers, especially acute lymphoblastic leukemia (ALL). One of the most significant side effects associated with asparaginase administration is immune suppression, which limits its application in clinic. Macrophages are phagocytic immune cells and have a central role in inflammation and host defense. We reported here that asparaginase disturbed the function of macrophages including phagocytosis, proliferation, ROS and nitric oxide secretion, interleukin 6 (IL-6) and tumor necrosis factor ? (TNF-?) secretion, and major histocompatibility complex II (MHC-II) molecule expression, thus induced immune suppression in interferon-? and lipopolysaccharide-stimulated macrophages. We also observed that asparaginase inhibited autophagy in macrophages via activating Akt/mTOR and suppressing Erk1/2 signaling pathway as evidenced by less formation of autophagosomes, downregulation of autophagy-related protein LC3-II, and decreased number of autophagy-like vacuoles. Further study discovered that treatment with autophagy inhibitor 3-MA in place of asparaginase on activated macrophages could also downregulate phagocytosis, cytokine secretion, and MHC-II expression. Moreover, incubation with autophagy inducer trehalose restored the capacity of phagocytosis, IL-6 and TNF-? secretion, and MHC-II expression in macrophages. These results prove the important role of autophagy in the function of macrophages, and activation of autophagy can overcome asparaginase-induced immune suppression in macrophages. äThe role of autophagy in asparaginase-induced immune suppression of ma(epmc).pdf DeepDyve Pubget Overpricing