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10.3389/fimmu.2021.686462 http://scihub22266oqcxt.onion/10.3389/fimmu.2021.686462 34276672!8278821!34276672     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       Front+Immunol 2021 ; 12 (ä): 686462 Nephropedia Template TP {{tp|p=34276672|t=2021. Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection |pdf=|usr=}}{{34276672}} gab.com Text Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34276672 #FOAvip Immune homeostasis is disturbed during severe viral infections, which can lead to loss of tolerance to self-peptides and result in short- or long-term autoimmunity. Using publicly available transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 52 autoantigens, known to be associated with 24 autoimmune diseases, during SAR-CoV-2 infection. Seven autoantigens (MPO, PRTN3, PADI4, IFIH1, TRIM21, PTPRN2, and TSHR) were upregulated in whole blood samples. MPO and TSHR were overexpressed in both lung autopsies and whole blood tissue and were associated with more severe COVID-19. Neutrophil activation derived autoantigens (MPO, PRTN3, and PADI4) were prominently increased in blood of both SARS-CoV-1 and SARS-CoV-2 viral infections, while TSHR and PTPRN2 autoantigens were specifically increased in SARS-CoV-2. Using single-cell dataset from peripheral blood mononuclear cells (PBMCs), we observed an upregulation of MPO, PRTN3, and PADI4 autoantigens within the low-density neutrophil subset. To validate our in-silico analysis, we measured plasma protein levels of two autoantigens, MPO and PRTN3, in severe and asymptomatic COVID-19. The protein levels of these two autoantigens were significantly upregulated in more severe COVID-19 infections. In conclusion, the immunopathology and severity of COVID-19 could result in transient autoimmune activation. Longitudinal follow-up studies of confirmed cases of COVID-19 could determine the enduring effects of viral infection including development of autoimmune disease. Twit Text FOAVip Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34276672 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34276672 #FOAvip English Wikipedia <ref>{{Cite pmid|34276672}}</ref> Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection #MMPMID34276672 Saheb Sharif-Askari N; Saheb Sharif-Askari F; Ahmed SBM; Hannawi S; Hamoudi R; Hamid Q; Halwani R Front Immunol 2021[]; 12 (ä): 686462 PMID34276672show ga Immune homeostasis is disturbed during severe viral infections, which can lead to loss of tolerance to self-peptides and result in short- or long-term autoimmunity. Using publicly available transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 52 autoantigens, known to be associated with 24 autoimmune diseases, during SAR-CoV-2 infection. Seven autoantigens (MPO, PRTN3, PADI4, IFIH1, TRIM21, PTPRN2, and TSHR) were upregulated in whole blood samples. MPO and TSHR were overexpressed in both lung autopsies and whole blood tissue and were associated with more severe COVID-19. Neutrophil activation derived autoantigens (MPO, PRTN3, and PADI4) were prominently increased in blood of both SARS-CoV-1 and SARS-CoV-2 viral infections, while TSHR and PTPRN2 autoantigens were specifically increased in SARS-CoV-2. Using single-cell dataset from peripheral blood mononuclear cells (PBMCs), we observed an upregulation of MPO, PRTN3, and PADI4 autoantigens within the low-density neutrophil subset. To validate our in-silico analysis, we measured plasma protein levels of two autoantigens, MPO and PRTN3, in severe and asymptomatic COVID-19. The protein levels of these two autoantigens were significantly upregulated in more severe COVID-19 infections. In conclusion, the immunopathology and severity of COVID-19 could result in transient autoimmune activation. Longitudinal follow-up studies of confirmed cases of COVID-19 could determine the enduring effects of viral infection including development of autoimmune disease. |*Transcriptome[MESH] |Asymptomatic Diseases[MESH] |Autoantigens/blood/*genetics[MESH] |Autoimmune Diseases/blood/immunology[MESH] |Autoimmunity/*genetics[MESH] |COVID-19/blood/*immunology/pathology/virology[MESH] |Computer Simulation[MESH] |Databases, Genetic[MESH] |Humans[MESH] |Lung/pathology[MESH] |Myeloblastin/blood/genetics[MESH] |Neutrophil Activation[MESH] |Neutrophils/immunology[MESH] |Peroxidase/blood/genetics[MESH] |RNA-Seq[MESH] |SARS-CoV-2/*immunology[MESH] |Severity of Illness Index[MESH]Enhanced Expression of Autoantigens During SARS-CoV-2 Viral Infection (epmc).pdf DeepDyve Pubget Overpricing