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10.1016/j.autrev.2020.102567 http://scihub22266oqcxt.onion/10.1016/j.autrev.2020.102567 32376392!7196557!32376392     free     free     free 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       Autoimmun+Rev 2020 ; 19 (7): 102567 Nephropedia Template TP {{tp|p=32376392|t=2020. Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions |pdf=|usr=}}{{32376392}} gab.com Text Should we stimulate or suppress immune responses in COVID-19 Cytokine and anti-cytokine interventions JO: Autoimmun Rev http://www.kidney.de/pget.php?&tw=1&pmid=32376392 #FOAvip The coronavirus disease-19 pandemic (COVID-19), which appeared in China in December 2019 and rapidly spread throughout the world, has forced clinicians and scientists to take up extraordinary challenges. This unprecedented situation led to the inception of numerous fundamental research protocols and many clinical trials. It quickly became apparent that although COVID-19, in the vast majority of cases, was a benign disease, it could also develop a severe form with sometimes fatal outcomes. Cytokines are central to the pathophysiology of COVID-19; while some of them are beneficial (type-I interferon, interleukin-7), others appear detrimental (interleukin-1beta, -6, and TNF-alpha) particularly in the context of the so-called cytokine storm. Yet another characteristic of the disease has emerged: concomitant immunodeficiency, notably involving impaired type-I interferon response, and lymphopenia. This review provides an overview of current knowledge on COVID-19 immunopathology. We discuss the defective type-I IFN response, the theoretical role of IL-7 to restore lymphocyte repertoire, as well as we mention the two patterns observed in severe COVID-19 (i.e. interleukin-1beta-driven macrophage activation syndrome vs. interleukin-6-driven immune dysregulation). Next, reviewing current evidence drawn from clinical trials, we examine a number of cytokine and anti-cytokine therapies, including interleukin-1, -6, and TNF inhibitors, as well as less targeted therapies, such as corticosteroids, chloroquine, or JAK inhibitors. Twit Text FOAVip Should we stimulate or suppress immune responses in COVID-19 Cytokine and anti-cytokine interventions ????Autoimmun Rev http://www.kidney.de/pget.php?&tw=1&pmid=32376392 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32376392 #FOAvip English Wikipedia <ref>{{Cite pmid|32376392}}</ref> Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions #MMPMID32376392 Jamilloux Y; Henry T; Belot A; Viel S; Fauter M; El Jammal T; Walzer T; Francois B; Seve P Autoimmun Rev 2020[Jul]; 19 (7): 102567 PMID32376392show ga The coronavirus disease-19 pandemic (COVID-19), which appeared in China in December 2019 and rapidly spread throughout the world, has forced clinicians and scientists to take up extraordinary challenges. This unprecedented situation led to the inception of numerous fundamental research protocols and many clinical trials. It quickly became apparent that although COVID-19, in the vast majority of cases, was a benign disease, it could also develop a severe form with sometimes fatal outcomes. Cytokines are central to the pathophysiology of COVID-19; while some of them are beneficial (type-I interferon, interleukin-7), others appear detrimental (interleukin-1beta, -6, and TNF-alpha) particularly in the context of the so-called cytokine storm. Yet another characteristic of the disease has emerged: concomitant immunodeficiency, notably involving impaired type-I interferon response, and lymphopenia. This review provides an overview of current knowledge on COVID-19 immunopathology. We discuss the defective type-I IFN response, the theoretical role of IL-7 to restore lymphocyte repertoire, as well as we mention the two patterns observed in severe COVID-19 (i.e. interleukin-1beta-driven macrophage activation syndrome vs. interleukin-6-driven immune dysregulation). Next, reviewing current evidence drawn from clinical trials, we examine a number of cytokine and anti-cytokine therapies, including interleukin-1, -6, and TNF inhibitors, as well as less targeted therapies, such as corticosteroids, chloroquine, or JAK inhibitors. |Betacoronavirus[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Coronavirus Infections/drug therapy/*immunology/*therapy[MESH] |Cytokines/*antagonists & inhibitors/*therapeutic use[MESH] |Humans[MESH] |Interferons/therapeutic use[MESH] |Interleukin-1beta[MESH] |Interleukin-6[MESH] |Pandemics[MESH] |Pneumonia, Viral/*immunology/*therapy[MESH]Should we stimulate or suppress immune responses in COVID-19? Cytokine(epmc).pdf DeepDyve Pubget Overpricing