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10.2147/ITT.S280706 http://scihub22266oqcxt.onion/10.2147/ITT.S280706 33728277!7955763!33728277     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunotargets+Ther 2021 ; 10 (ä): 63-85 Nephropedia Template TP {{tp|p=33728277|t=2021. Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches |pdf=|usr=}}{{33728277}} gab.com Text Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches JO: Immunotargets Ther http://www.kidney.de/pget.php?&tw=1&pmid=33728277 #FOAvip Coronavirus disease 2019 (Covid-19), caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can range in severity from asymptomatic to severe/critical disease. SARS-CoV-2 uses angiotensin-converting enzyme 2 to infect cells leading to a strong inflammatory response, which is most profound in patients who progress to severe Covid-19. Recent studies have begun to unravel some of the differences in the innate and adaptive immune response to SARS-CoV-2 in patients with different degrees of disease severity. These studies have attributed the severe form of Covid-19 to a dysfunctional innate immune response, such as a delayed and/or deficient type I interferon response, coupled with an exaggerated and/or a dysfunctional adaptive immunity. Differences in T-cell (including CD4(+) T-cells, CD8(+) T-cells, T follicular helper cells, gammadelta-T-cells, and regulatory T-cells) and B-cell (transitional cells, double-negative 2 cells, antibody-secreting cells) responses have been identified in patients with severe disease compared to mild cases. Moreover, differences in the kinetic/titer of neutralizing antibody responses have been described in severe disease, which may be confounded by antibody-dependent enhancement. Importantly, the presence of preexisting autoantibodies against type I interferon has been described as a major cause of severe/critical disease. Additionally, priorVaccine and multiple vaccine exposure, trained innate immunity, cross-reactive immunity, and serological immune imprinting may all contribute towards disease severity and outcome. Several therapeutic and preventative approaches have been under intense investigations; these include vaccines (three of which have passed Phase 3 clinical trials), therapeutic antibodies, and immunosuppressants. Twit Text FOAVip Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches ????Immunotargets Ther http://www.kidney.de/pget.php?&tw=1&pmid=33728277 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33728277 #FOAvip English Wikipedia <ref>{{Cite pmid|33728277}}</ref> Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches #MMPMID33728277 Hasan A; Al-Ozairi E; Al-Baqsumi Z; Ahmad R; Al-Mulla F Immunotargets Ther 2021[]; 10 (ä): 63-85 PMID33728277show ga Coronavirus disease 2019 (Covid-19), caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can range in severity from asymptomatic to severe/critical disease. SARS-CoV-2 uses angiotensin-converting enzyme 2 to infect cells leading to a strong inflammatory response, which is most profound in patients who progress to severe Covid-19. Recent studies have begun to unravel some of the differences in the innate and adaptive immune response to SARS-CoV-2 in patients with different degrees of disease severity. These studies have attributed the severe form of Covid-19 to a dysfunctional innate immune response, such as a delayed and/or deficient type I interferon response, coupled with an exaggerated and/or a dysfunctional adaptive immunity. Differences in T-cell (including CD4(+) T-cells, CD8(+) T-cells, T follicular helper cells, gammadelta-T-cells, and regulatory T-cells) and B-cell (transitional cells, double-negative 2 cells, antibody-secreting cells) responses have been identified in patients with severe disease compared to mild cases. Moreover, differences in the kinetic/titer of neutralizing antibody responses have been described in severe disease, which may be confounded by antibody-dependent enhancement. Importantly, the presence of preexisting autoantibodies against type I interferon has been described as a major cause of severe/critical disease. Additionally, priorVaccine and multiple vaccine exposure, trained innate immunity, cross-reactive immunity, and serological immune imprinting may all contribute towards disease severity and outcome. Several therapeutic and preventative approaches have been under intense investigations; these include vaccines (three of which have passed Phase 3 clinical trials), therapeutic antibodies, and immunosuppressants. äCellular and Humoral Immune Responses in Covid-19 and Immunotherapeuti(epmc).pdf DeepDyve Pubget Overpricing