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10.1136/annrheumdis-2013-204343 http://scihub22266oqcxt.onion/10.1136/annrheumdis-2013-204343 C4152192!4152192!24419333     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+Rheum+Dis 2015 ; 74 (5): 912-20 Nephropedia Template TP {{tp|p=24419333|t=2015. Autophagy is activated in systemic lupus erythematosus and required for plasmablast development |pdf=|usr=}}{{24419333}} gab.com Text Autophagy is activated in systemic lupus erythematosus and required for plasmablast development JO: Ann Rheum Dis http://www.kidney.de/pget.php?&tw=1&pmid=24419333 #FOAvip Background: Autophagy has emerged as a critical homeostatic mechanism in T lymphocytes, influencing proliferation and differentiation. Autophagy in B cells has been less studied, but genetic deficiency causes impairment of early and late developmental stages Objectives: To explore the role of autophagy in the pathogenesis of human and murine lupus, a disease in which B cells are critical effectors of pathology. Methods: Autophagy was assessed using multiple techniques in NZB/W and control mice, and in patients with systemic lupus erythematosus (SLE) compared to healthy controls. We evaluated the phenotype of the B cell compartment in Vav-Atg7?/? mice in vivo, and examined human and murine plasmablast formation following inhibition of autophagy. Results: We found activation of autophagy in early developmental and transitional stages of B cell development in a lupus mouse model even before disease onset, and which progressively increased with age. In human disease, again autophagy was activated compared with healthy controls, principally in naïve B cells. B cells isolated from Vav-Atg7F/F mice failed to effectively differentiate into plasma cells following stimulation in vitro. Similarly, human B cells stimulated in the presence of autophagy inhibition did not differentiate into plasmablasts. Conclusions: Our data suggest activation of autophagy is a mechanism for survival of autoreactive B cells, and also demonstrate that it is required for plasmablast differentiation, processes that induce significant cellular stress. The implication of autophagy in two major pathogenic pathways in SLE suggests the potential to use inhibition of autophagy as a novel treatment target in this frequently severe autoimmune disease. Twit Text FOAVip Autophagy is activated in systemic lupus erythematosus and required for plasmablast development ????Ann Rheum Dis http://www.kidney.de/pget.php?&tw=1&pmid=24419333 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24419333 #FOAvip English Wikipedia <ref>{{Cite pmid|24419333}}</ref> Autophagy is activated in systemic lupus erythematosus and required for plasmablast development #MMPMID24419333 Clarke AJ; Ellinghaus U; Cortini A; Stranks A; Simon AK; Botto M; Vyse TJ Ann Rheum Dis 2015[May]; 74 (5): 912-20 PMID24419333show ga Background: Autophagy has emerged as a critical homeostatic mechanism in T lymphocytes, influencing proliferation and differentiation. Autophagy in B cells has been less studied, but genetic deficiency causes impairment of early and late developmental stages Objectives: To explore the role of autophagy in the pathogenesis of human and murine lupus, a disease in which B cells are critical effectors of pathology. Methods: Autophagy was assessed using multiple techniques in NZB/W and control mice, and in patients with systemic lupus erythematosus (SLE) compared to healthy controls. We evaluated the phenotype of the B cell compartment in Vav-Atg7?/? mice in vivo, and examined human and murine plasmablast formation following inhibition of autophagy. Results: We found activation of autophagy in early developmental and transitional stages of B cell development in a lupus mouse model even before disease onset, and which progressively increased with age. In human disease, again autophagy was activated compared with healthy controls, principally in naïve B cells. B cells isolated from Vav-Atg7F/F mice failed to effectively differentiate into plasma cells following stimulation in vitro. Similarly, human B cells stimulated in the presence of autophagy inhibition did not differentiate into plasmablasts. Conclusions: Our data suggest activation of autophagy is a mechanism for survival of autoreactive B cells, and also demonstrate that it is required for plasmablast differentiation, processes that induce significant cellular stress. The implication of autophagy in two major pathogenic pathways in SLE suggests the potential to use inhibition of autophagy as a novel treatment target in this frequently severe autoimmune disease. äAutophagy is activated in systemic lupus erythematosus and required fo(epmc).pdf DeepDyve Pubget Overpricing