Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.3389/fimmu.2021.714511

http://scihub22266oqcxt.onion/10.3389/fimmu.2021.714511
suck pdf from google scholar
34290717!8287855!34290717
unlimited free pdf from europmc34290717    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
pmid34290717      Front+Immunol 2021 ; 12 (ä): 714511
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Lectin Pathway Mediates Complement Activation by SARS-CoV-2 Proteins #MMPMID34290717
  • Ali YM; Ferrari M; Lynch NJ; Yaseen S; Dudler T; Gragerov S; Demopulos G; Heeney JL; Schwaeble WJ
  • Front Immunol 2021[]; 12 (ä): 714511 PMID34290717show ga
  • Early and persistent activation of complement is considered to play a key role in the pathogenesis of COVID-19. Complement activation products orchestrate a proinflammatory environment that might be critical for the induction and maintenance of a severe inflammatory response to SARS-CoV-2 by recruiting cells of the cellular immune system to the sites of infection and shifting their state of activation towards an inflammatory phenotype. It precedes pathophysiological milestone events like the cytokine storm, progressive endothelial injury triggering microangiopathy, and further complement activation, and causes an acute respiratory distress syndrome (ARDS). To date, the application of antiviral drugs and corticosteroids have shown efficacy in the early stages of SARS-CoV-2 infection, but failed to ameliorate disease severity in patients who progressed to severe COVID-19 pathology. This report demonstrates that lectin pathway (LP) recognition molecules of the complement system, such as MBL, FCN-2 and CL-11, bind to SARS-CoV-2 S- and N-proteins, with subsequent activation of LP-mediated C3b and C4b deposition. In addition, our results confirm and underline that the N-protein of SARS-CoV-2 binds directly to the LP- effector enzyme MASP-2 and activates complement. Inhibition of the LP using an inhibitory monoclonal antibody against MASP-2 effectively blocks LP-mediated complement activation. FACS analyses using transfected HEK-293 cells expressing SARS-CoV-2 S protein confirm a robust LP-dependent C3b deposition on the cell surface which is inhibited by the MASP-2 inhibitory antibody. In light of our present results, and the encouraging performance of our clinical candidate MASP-2 inhibitor Narsoplimab in recently published clinical trials, we suggest that the targeting of MASP-2 provides an unsurpassed window of therapeutic efficacy for the treatment of severe COVID-19.
  • |Adult[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Asian People[MESH]
  • |Biomarkers/blood[MESH]
  • |COVID-19/*blood/complications/pathology/physiopathology[MESH]
  • |Cohort Studies[MESH]
  • |Complement Activation/*immunology[MESH]
  • |Complement System Proteins/immunology/*metabolism[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Lectins/*blood[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Renal Insufficiency, Chronic/complications/*metabolism/virology[MESH]
  • |SARS-CoV-2/*metabolism[MESH]
  • |Severity of Illness Index[MESH]
  • |Spike Glycoprotein, Coronavirus/*metabolism[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box