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10.1038/s41586-021-04280-x http://scihub22266oqcxt.onion/10.1038/s41586-021-04280-x 34875673!8810382!34875673     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34875673&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       Nature 2022 ; 602 (7895): 148-155 Nephropedia Template TP {{tp|p=34875673|t=2022. Signature of long-lived memory CD8(+) T cells in acute SARS-CoV-2 infection |pdf=|usr=}}{{34875673}} gab.com Text Signature of long-lived memory CD8(+) T cells in acute SARS-CoV-2 infection JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=34875673 #FOAvip Immunological memory is a hallmark of adaptive immunity and facilitates an accelerated and enhanced immune response upon re-infection with the same pathogen(1,2). Since the outbreak of the ongoing COVID-19 pandemic, a key question has focused on which SARS-CoV-2-specific T cells stimulated during acute infection give rise to long-lived memory T cells(3). Here, using spectral flow cytometry combined with cellular indexing of transcriptomes and T cell receptor sequencing, we longitudinally characterized individual SARS-CoV-2-specific CD8(+) T cells of patients with COVID-19 from acute infection to 1 year into recovery and found a distinct signature identifying long-lived memory CD8(+) T cells. SARS-CoV-2-specific memory CD8(+) T cells persisting 1 year after acute infection express CD45RA, IL-7 receptor-alpha and T cell factor 1, but they maintain low expression of CCR7, thus resembling CD45RA(+) effector memory T cells. Tracking individual clones of SARS-CoV-2-specific CD8(+) T cells, we reveal that an interferon signature marks clones that give rise to long-lived cells, whereas prolonged proliferation and mechanistic target of rapamycin signalling are associated with clonal disappearance from the blood. Collectively, we describe a transcriptional signature that marks long-lived, circulating human memory CD8(+) T cells following an acute viral infection. Twit Text FOAVip Signature of long-lived memory CD8(+) T cells in acute SARS-CoV-2 infection ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=34875673 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34875673 #FOAvip English Wikipedia <ref>{{Cite pmid|34875673}}</ref> Signature of long-lived memory CD8(+) T cells in acute SARS-CoV-2 infection #MMPMID34875673 Adamo S; Michler J; Zurbuchen Y; Cervia C; Taeschler P; Raeber ME; Baghai Sain S; Nilsson J; Moor AE; Boyman O Nature 2022[Feb]; 602 (7895): 148-155 PMID34875673show ga Immunological memory is a hallmark of adaptive immunity and facilitates an accelerated and enhanced immune response upon re-infection with the same pathogen(1,2). Since the outbreak of the ongoing COVID-19 pandemic, a key question has focused on which SARS-CoV-2-specific T cells stimulated during acute infection give rise to long-lived memory T cells(3). Here, using spectral flow cytometry combined with cellular indexing of transcriptomes and T cell receptor sequencing, we longitudinally characterized individual SARS-CoV-2-specific CD8(+) T cells of patients with COVID-19 from acute infection to 1 year into recovery and found a distinct signature identifying long-lived memory CD8(+) T cells. SARS-CoV-2-specific memory CD8(+) T cells persisting 1 year after acute infection express CD45RA, IL-7 receptor-alpha and T cell factor 1, but they maintain low expression of CCR7, thus resembling CD45RA(+) effector memory T cells. Tracking individual clones of SARS-CoV-2-specific CD8(+) T cells, we reveal that an interferon signature marks clones that give rise to long-lived cells, whereas prolonged proliferation and mechanistic target of rapamycin signalling are associated with clonal disappearance from the blood. Collectively, we describe a transcriptional signature that marks long-lived, circulating human memory CD8(+) T cells following an acute viral infection. |Acute Disease[MESH] |Antigens, Viral/*immunology[MESH] |Biomarkers/*metabolism[MESH] |CD8-Positive T-Lymphocytes/*immunology/*metabolism[MESH] |COVID-19/*immunology/virology[MESH] |Cell Proliferation[MESH] |Clone Cells/cytology/immunology[MESH] |Humans[MESH] |Interferons/immunology[MESH] |Interleukin-7 Receptor alpha Subunit/metabolism[MESH] |Leukocyte Common Antigens/metabolism[MESH] |Longitudinal Studies[MESH] |Mechanistic Target of Rapamycin Complex 1/metabolism[MESH] |Memory T Cells/*immunology/*metabolism[MESH] |Receptors, Antigen, T-Cell/metabolism[MESH] |Receptors, CCR7/metabolism[MESH] |SARS-CoV-2/*immunology[MESH] |T Cell Transcription Factor 1/metabolism[MESH] |Time Factors[MESH]Signature of long-lived memory CD8(+) T cells in acute SARS-CoV-2 infe(epmc).pdf DeepDyve Pubget Overpricing