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.

10.1016/j.immuni.2021.05.006 http://scihub22266oqcxt.onion/10.1016/j.immuni.2021.05.006 34048708!8106883!34048708     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34048708&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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 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 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34048708.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Immunity 2021 ; 54 (6): 1304-1319.e9 Nephropedia Template TP {{tp|p=34048708|t=2021. SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2 |pdf=|usr=}}{{34048708}} gab.com Text SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2 JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=34048708 #FOAvip Despite mounting evidence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) engagement with immune cells, most express little, if any, of the canonical receptor of SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2). Here, using a myeloid cell receptor-focused ectopic expression screen, we identified several C-type lectins (DC-SIGN, L-SIGN, LSECtin, ASGR1, and CLEC10A) and Tweety family member 2 (TTYH2) as glycan-dependent binding partners of the SARS-CoV-2 spike. Except for TTYH2, these molecules primarily interacted with spike via regions outside of the receptor-binding domain. Single-cell RNA sequencing analysis of pulmonary cells from individuals with coronavirus disease 2019 (COVID-19) indicated predominant expression of these molecules on myeloid cells. Although these receptors do not support active replication of SARS-CoV-2, their engagement with the virus induced robust proinflammatory responses in myeloid cells that correlated with COVID-19 severity. We also generated a bispecific anti-spike nanobody that not only blocked ACE2-mediated infection but also the myeloid receptor-mediated proinflammatory responses. Our findings suggest that SARS-CoV-2-myeloid receptor interactions promote immune hyperactivation, which represents potential targets for COVID-19 therapy. Twit Text FOAVip SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2 ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=34048708 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34048708 #FOAvip English Wikipedia <ref>{{Cite pmid|34048708}}</ref> SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2 #MMPMID34048708 Lu Q; Liu J; Zhao S; Gomez Castro MF; Laurent-Rolle M; Dong J; Ran X; Damani-Yokota P; Tang H; Karakousi T; Son J; Kaczmarek ME; Zhang Z; Yeung ST; McCune BT; Chen RE; Tang F; Ren X; Chen X; Hsu JCC; Teplova M; Huang B; Deng H; Long Z; Mudianto T; Jin S; Lin P; Du J; Zang R; Su TT; Herrera A; Zhou M; Yan R; Cui J; Zhu J; Zhou Q; Wang T; Ma J; Koralov SB; Zhang Z; Aifantis I; Segal LN; Diamond MS; Khanna KM; Stapleford KA; Cresswell P; Liu Y; Ding S; Xie Q; Wang J Immunity 2021[Jun]; 54 (6): 1304-1319.e9 PMID34048708show ga Despite mounting evidence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) engagement with immune cells, most express little, if any, of the canonical receptor of SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2). Here, using a myeloid cell receptor-focused ectopic expression screen, we identified several C-type lectins (DC-SIGN, L-SIGN, LSECtin, ASGR1, and CLEC10A) and Tweety family member 2 (TTYH2) as glycan-dependent binding partners of the SARS-CoV-2 spike. Except for TTYH2, these molecules primarily interacted with spike via regions outside of the receptor-binding domain. Single-cell RNA sequencing analysis of pulmonary cells from individuals with coronavirus disease 2019 (COVID-19) indicated predominant expression of these molecules on myeloid cells. Although these receptors do not support active replication of SARS-CoV-2, their engagement with the virus induced robust proinflammatory responses in myeloid cells that correlated with COVID-19 severity. We also generated a bispecific anti-spike nanobody that not only blocked ACE2-mediated infection but also the myeloid receptor-mediated proinflammatory responses. Our findings suggest that SARS-CoV-2-myeloid receptor interactions promote immune hyperactivation, which represents potential targets for COVID-19 therapy. |*Host-Pathogen Interactions/genetics/immunology[MESH] |Angiotensin-Converting Enzyme 2/metabolism[MESH] |Binding Sites[MESH] |COVID-19/genetics/*metabolism/*virology[MESH] |Cell Line[MESH] |Cytokines[MESH] |Gene Expression Regulation[MESH] |Humans[MESH] |Inflammation Mediators/metabolism[MESH] |Lectins, C-Type/chemistry/*metabolism[MESH] |Membrane Proteins/chemistry/*metabolism[MESH] |Models, Molecular[MESH] |Myeloid Cells/*immunology/*metabolism[MESH] |Neoplasm Proteins/chemistry/*metabolism[MESH] |Protein Binding[MESH] |Protein Conformation[MESH] |SARS-CoV-2/*physiology[MESH] |Single-Domain Antibodies/immunology[MESH] |Spike Glycoprotein, Coronavirus/chemistry/immunology/metabolism[MESH]SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells thro(epmc).pdf DeepDyve Pubget Overpricing