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10.1016/j.cell.2021.12.040 http://scihub22266oqcxt.onion/10.1016/j.cell.2021.12.040 35032429!8712270!35032429     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35032429&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 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2022 ; 185 (3): 493-512.e25 Nephropedia Template TP {{tp|p=35032429|t=2022. Complement activation induces excessive T cell cytotoxicity in severe COVID-19 |pdf=|usr=}}{{35032429}} gab.com Text Complement activation induces excessive T cell cytotoxicity in severe COVID-19 JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=35032429 #FOAvip Severe COVID-19 is linked to both dysfunctional immune response and unrestrained immunopathology, and it remains unclear whether T cells contribute to disease pathology. Here, we combined single-cell transcriptomics and single-cell proteomics with mechanistic studies to assess pathogenic T cell functions and inducing signals. We identified highly activated CD16(+) T cells with increased cytotoxic functions in severe COVID-19. CD16 expression enabled immune-complex-mediated, T cell receptor-independent degranulation and cytotoxicity not found in other diseases. CD16(+) T cells from COVID-19 patients promoted microvascular endothelial cell injury and release of neutrophil and monocyte chemoattractants. CD16(+) T cell clones persisted beyond acute disease maintaining their cytotoxic phenotype. Increased generation of C3a in severe COVID-19 induced activated CD16(+) cytotoxic T cells. Proportions of activated CD16(+) T cells and plasma levels of complement proteins upstream of C3a were associated with fatal outcome of COVID-19, supporting a pathological role of exacerbated cytotoxicity and complement activation in COVID-19. Twit Text FOAVip Complement activation induces excessive T cell cytotoxicity in severe COVID-19 ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=35032429 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35032429 #FOAvip English Wikipedia <ref>{{Cite pmid|35032429}}</ref> Complement activation induces excessive T cell cytotoxicity in severe COVID-19 #MMPMID35032429 Georg P; Astaburuaga-Garcia R; Bonaguro L; Brumhard S; Michalick L; Lippert LJ; Kostevc T; Gabel C; Schneider M; Streitz M; Demichev V; Gemund I; Barone M; Tober-Lau P; Helbig ET; Hillus D; Petrov L; Stein J; Dey HP; Paclik D; Iwert C; Mulleder M; Aulakh SK; Djudjaj S; Bulow RD; Mei HE; Schulz AR; Thiel A; Hippenstiel S; Saliba AE; Eils R; Lehmann I; Mall MA; Stricker S; Rohmel J; Corman VM; Beule D; Wyler E; Landthaler M; Obermayer B; von Stillfried S; Boor P; Demir M; Wesselmann H; Suttorp N; Uhrig A; Muller-Redetzky H; Nattermann J; Kuebler WM; Meisel C; Ralser M; Schultze JL; Aschenbrenner AC; Thibeault C; Kurth F; Sander LE; Bluthgen N; Sawitzki B Cell 2022[Feb]; 185 (3): 493-512.e25 PMID35032429show ga Severe COVID-19 is linked to both dysfunctional immune response and unrestrained immunopathology, and it remains unclear whether T cells contribute to disease pathology. Here, we combined single-cell transcriptomics and single-cell proteomics with mechanistic studies to assess pathogenic T cell functions and inducing signals. We identified highly activated CD16(+) T cells with increased cytotoxic functions in severe COVID-19. CD16 expression enabled immune-complex-mediated, T cell receptor-independent degranulation and cytotoxicity not found in other diseases. CD16(+) T cells from COVID-19 patients promoted microvascular endothelial cell injury and release of neutrophil and monocyte chemoattractants. CD16(+) T cell clones persisted beyond acute disease maintaining their cytotoxic phenotype. Increased generation of C3a in severe COVID-19 induced activated CD16(+) cytotoxic T cells. Proportions of activated CD16(+) T cells and plasma levels of complement proteins upstream of C3a were associated with fatal outcome of COVID-19, supporting a pathological role of exacerbated cytotoxicity and complement activation in COVID-19. |*Complement Activation[MESH] |*Proteome[MESH] |*Transcriptome[MESH] |Adult[MESH] |Aged[MESH] |Aged, 80 and over[MESH] |COVID-19/*immunology/*pathology/virology[MESH] |Chemotactic Factors/metabolism[MESH] |Cytotoxicity, Immunologic[MESH] |Endothelial Cells/virology[MESH] |Female[MESH] |Humans[MESH] |Lymphocyte Activation[MESH] |Male[MESH] |Microvessels/virology[MESH] |Middle Aged[MESH] |Monocytes/metabolism[MESH] |Neutrophils/metabolism[MESH] |Receptors, IgG/metabolism[MESH] |SARS-CoV-2/*immunology[MESH] |Single-Cell Analysis[MESH] |T-Lymphocytes, Cytotoxic/*immunology[MESH]Complement activation induces excessive T cell cytotoxicity in severe (epmc).pdf DeepDyve Pubget Overpricing