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10.1016/j.mehy.2020.110345

http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.110345
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suck abstract from ncbi


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pmid33080459      Med+Hypotheses 2020 ; 145 (ä): 110345
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  • The triggering of post-COVID-19 autoimmunity phenomena could be associated with both transient immunosuppression and an inappropriate form of immune reconstitution in susceptible individuals #MMPMID33080459
  • Canas CA
  • Med Hypotheses 2020[Dec]; 145 (ä): 110345 PMID33080459show ga
  • With the progression of the COVID-19 pandemic, there have been different reports about the development of autoimmune diseases once the infection is controlled. After entering the respiratory epithelial cells, SARS-CoV-2-the virus that causes the disease-triggers a severe inflammatory state in some patients known as "cytokine storm" and the development of thrombotic phenomena-both conditions being associated with high mortality. Patients additionally present severe lymphopenia and, in some cases, complement consumption and autoantibody development. There is a normalization of lymphocytes once the infection is controlled. After this, autoimmune conditions of unknown etiology may occur. A hypothesis for the development of post-COVID-19 autoimmunity is proposed based on the consequences of both a transient immunosuppression (both of innate and acquired immunity) in which self-tolerance is lost and an inappropriate form of immune reconstitution that amplifies the process.
  • |Adaptive Immunity[MESH]
  • |Autoantibodies/chemistry[MESH]
  • |Autoantigens[MESH]
  • |Autoimmunity/*immunology[MESH]
  • |COVID-19/blood/*immunology[MESH]
  • |Cytokines/immunology[MESH]
  • |Disease Progression[MESH]
  • |Disease Susceptibility[MESH]
  • |Humans[MESH]
  • |Immune Reconstitution[MESH]
  • |Immune Tolerance[MESH]
  • |Immunity, Innate[MESH]
  • |Immunosuppression Therapy[MESH]
  • |Inflammation[MESH]
  • |Lymphocytes/immunology[MESH]
  • |Models, Theoretical[MESH]


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