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10.1016/bs.ai.2021.08.002 http://scihub22266oqcxt.onion/10.1016/bs.ai.2021.08.002 34656288!8429035!34656288     free     free     free       Adv+Immunol 2021 ; 151 (ä): 49-97 Nephropedia Template TP {{tp|p=34656288|t=2021. Immunology of SARS-CoV-2 infections and vaccines |pdf=|usr=}}{{34656288}} gab.com Text Immunology of SARS-CoV-2 infections and vaccines JO: Adv Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34656288 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections trigger viral RNA sensors such as TLR7 and RIG-I, thereby leading to production of type I interferon (IFN) and other inflammatory mediators. Expression of viral proteins in the context of this inflammation leads to stereotypical antigen-specific antibody and T cell responses that clear the virus. Immunity is then maintained through long-lived antibody-secreting plasma cells and by memory B and T cells that can initiate anamnestic responses. Each of these steps is consistent with prior knowledge of acute RNA virus infections. Yet there are certain concepts, while not entirely new, that have been resurrected by the biology of severe SARS-CoV-2 infections and deserve further attention. These include production of anti-IFN autoantibodies, early inflammatory processes that slow adaptive humoral immunity, immunodominance of antibody responses, and original antigenic sin. Moreover, multiple different vaccine platforms allow for comparisons of pathways that promote robust and durable adaptive immunity. Twit Text FOAVip Immunology of SARS-CoV-2 infections and vaccines ????Adv Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34656288 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34656288 #FOAvip English Wikipedia <ref>{{Cite pmid|34656288}}</ref> Immunology of SARS-CoV-2 infections and vaccines #MMPMID34656288 Schenten D; Bhattacharya D Adv Immunol 2021[]; 151 (ä): 49-97 PMID34656288show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections trigger viral RNA sensors such as TLR7 and RIG-I, thereby leading to production of type I interferon (IFN) and other inflammatory mediators. Expression of viral proteins in the context of this inflammation leads to stereotypical antigen-specific antibody and T cell responses that clear the virus. Immunity is then maintained through long-lived antibody-secreting plasma cells and by memory B and T cells that can initiate anamnestic responses. Each of these steps is consistent with prior knowledge of acute RNA virus infections. Yet there are certain concepts, while not entirely new, that have been resurrected by the biology of severe SARS-CoV-2 infections and deserve further attention. These include production of anti-IFN autoantibodies, early inflammatory processes that slow adaptive humoral immunity, immunodominance of antibody responses, and original antigenic sin. Moreover, multiple different vaccine platforms allow for comparisons of pathways that promote robust and durable adaptive immunity. |*COVID-19[MESH] |*Vaccines[MESH] |Adaptive Immunity[MESH] |Humans[MESH] |Immunity, Humoral[MESH]Immunology of SARS-CoV-2 infections and vaccines (epmc).pdf DeepDyve Pubget Overpricing