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1.
Scand J Immunol ; 93(4): e12998, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33190302

RESUMO

SARS-CoV-2 is a novel human coronavirus responsible for the Coronavirus disease 2019 (COVID-19) pandemic. Pneumonia and acute respiratory distress syndrome are the major complications of COVID-19. SARS-CoV-2 infection can activate innate and adaptive immune responses and result in massive inflammatory responses later in the disease. These uncontrolled inflammatory responses may lead to local and systemic tissue damage. In patients with severe COVID-19, eosinopenia and lymphopenia with a severe reduction in the frequency of CD4+ and CD8+ T cells, B cells and natural killer (NK) cells are a common feature. COVID-19 severity hinges on the development of cytokine storm characterized by elevated serum levels of pro-inflammatory cytokines. Moreover, IgG-, IgM- and IgA-specific antibodies against SARS-CoV-2 can be detected in most patients, along with the viral RNA, forming the basis for assays that aid in patient diagnosis. Elucidating the immunopathological outcomes due to COVID-19 could provide potential targets for immunotherapy and are important for choosing the best clinical management by consultants. Currently, along with standard supportive care, therapeutic approaches to COVID-19 treatment involve the use of antiviral agents that interfere with the SARS-CoV-2 lifecycle to prevent further viral replication and utilizing immunomodulators to dampen the immune system in order to prevent cytokine storm and tissue damage. While current therapeutic options vary in efficacy, there are several molecules that were either shown to be effective against other viruses such as HIV or show promise in vitro that could be added to the growing arsenal of agents used to control COVID-19 severity and spread.


Assuntos
Antivirais/uso terapêutico , COVID-19/imunologia , Fatores Imunológicos/uso terapêutico , SARS-CoV-2/fisiologia , COVID-19/diagnóstico , COVID-19/terapia , Teste Sorológico para COVID-19 , Síndrome da Liberação de Citocina , Humanos , Linfopenia , Pandemias , Síndrome do Desconforto Respiratório , Replicação Viral , Tratamento Farmacológico da COVID-19
2.
Nat Commun ; 10(1): 705, 2019 02 11.
Artigo em Inglês | MEDLINE | ID: mdl-30741936

RESUMO

TRADD is an adaptor for TNFR1-induced apoptosis and NFκB activation. However, TRADD-deficient mice undergo normal development and contain normal lymphoid populations, which contrasts with an embryonic defect in mice lacking FADD, the shared adaptor mediating apoptosis. Recent studies indicate FADD suppresses embryonic necroptosis mediated by RIPK1. TRADD was suggested to also mediate necroptosis. Here we report that targeting TRADD fails to rescue Fadd-/- embryos from necroptosis, and ablation of TRADD rescues Ripk1-/- mice from perinatal lethality when RIPK3-mediated necroptosis is disabled. The resulting Ripk1-/-Ripk3-/-Tradd-/- mice survive until early adulthood, but die thereafter. A single allele of Tradd is optimal for survival of Ripk1-/-Ripk3-/-Tradd+/- mice. We show that TRADD plays a more dominating role in NFκB-signaling than RIPK1. While RIPK1 protects thymocytes from TNFα-induced apoptosis, TRADD promotes this process. The data demonstrate that TRADD is critical in perinatal and adult mice lacking RIPK1 and RIPK3, which has not been appreciated in prior studies.


Assuntos
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo , Proteína de Domínio de Morte Associada a Receptor de TNF/metabolismo , Animais , Apoptose/efeitos dos fármacos , Caspase 8/genética , Caspase 8/metabolismo , Morte Celular , Proliferação de Células/efeitos dos fármacos , Proteína de Domínio de Morte Associada a Fas/metabolismo , Fibroblastos , Deleção de Genes , Regulação da Expressão Gênica , Intestinos/patologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , NF-kappa B , Necrose , Proteína Serina-Treonina Quinases de Interação com Receptores/genética , Proteína Serina-Treonina Quinases de Interação com Receptores/farmacologia , Transdução de Sinais , Análise de Sobrevida , Linfócitos T/efeitos dos fármacos , Linfócitos T/metabolismo , Proteína de Domínio de Morte Associada a Receptor de TNF/genética , Proteína de Domínio de Morte Associada a Receptor de TNF/farmacologia , Timócitos/efeitos dos fármacos , Transcriptoma , Fator de Necrose Tumoral alfa
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