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10.1016/j.ajpath.2020.08.009 http://scihub22266oqcxt.onion/10.1016/j.ajpath.2020.08.009 32919977!7484812!32919977     free     free     free       Am+J+Pathol 2021 ; 191 (1): 4-17 Nephropedia Template TP {{tp|p=32919977|t=2021. Immunopathology of Hyperinflammation in COVID-19 |pdf=|usr=}}{{32919977}} gab.com Text Immunopathology of Hyperinflammation in COVID-19 JO: Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=32919977 #FOAvip The rapid spread of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), has resulted in an unprecedented public health crisis worldwide. Recent studies indicate that a hyperinflammatory syndrome induced by SARS-CoV-2 contributes to disease severity and mortality in COVID-19. In this review, an overview of the pathophysiology underlying the hyperinflammatory syndrome in severe COVID-19 is provided. The current evidence suggests that the hyperinflammatory syndrome results from a dysregulated host innate immune response. The gross and microscopic pathologic findings as well as the alterations in the cytokine milieu, macrophages/monocytes, natural killer cells, T cells, and neutrophils in severe COVID-19 are summarized. The data highlighted include the potential therapeutic approaches undergoing investigation to modulate the immune response and abrogate lung injury in severe COVID-19. Twit Text FOAVip Immunopathology of Hyperinflammation in COVID-19 ????Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=32919977 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32919977 #FOAvip English Wikipedia <ref>{{Cite pmid|32919977}}</ref> Immunopathology of Hyperinflammation in COVID-19 #MMPMID32919977 Gustine JN; Jones D Am J Pathol 2021[Jan]; 191 (1): 4-17 PMID32919977show ga The rapid spread of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), has resulted in an unprecedented public health crisis worldwide. Recent studies indicate that a hyperinflammatory syndrome induced by SARS-CoV-2 contributes to disease severity and mortality in COVID-19. In this review, an overview of the pathophysiology underlying the hyperinflammatory syndrome in severe COVID-19 is provided. The current evidence suggests that the hyperinflammatory syndrome results from a dysregulated host innate immune response. The gross and microscopic pathologic findings as well as the alterations in the cytokine milieu, macrophages/monocytes, natural killer cells, T cells, and neutrophils in severe COVID-19 are summarized. The data highlighted include the potential therapeutic approaches undergoing investigation to modulate the immune response and abrogate lung injury in severe COVID-19. |*Cytokine Release Syndrome[MESH] |*Immune System[MESH] |*Inflammation[MESH] |Adrenal Cortex Hormones/therapeutic use[MESH] |COVID-19/epidemiology/*immunology/therapy[MESH] |Extracellular Traps[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Killer Cells, Natural/immunology[MESH] |Macrophage Activation[MESH] |Macrophages/immunology[MESH] |Monocytes/immunology[MESH] |Neutrophils/immunology[MESH] |Phagocytosis[MESH] |SARS-CoV-2/physiology[MESH] |Systemic Inflammatory Response Syndrome/*epidemiology[MESH] |T-Lymphocytes/immunology[MESH]Immunopathology of Hyperinflammation in COVID-19 (epmc).pdf DeepDyve Pubget Overpricing