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

Med Hypotheses. 2020 Dec:145:110345. doi: 10.1016/j.mehy.2020.110345. Epub 2020 Oct 14.

Abstract

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.

Keywords: Autoimmune disease; Autoimmunity; COVID-19; Immune response; SARS-CoV-2.

MeSH terms

  • Adaptive Immunity
  • Autoantibodies / chemistry
  • Autoantigens
  • Autoimmunity / immunology*
  • COVID-19 / blood
  • COVID-19 / immunology*
  • Cytokines / immunology
  • Disease Progression
  • Disease Susceptibility
  • Humans
  • Immune Reconstitution
  • Immune Tolerance
  • Immunity, Innate
  • Immunosuppression Therapy
  • Inflammation
  • Lymphocytes / immunology
  • Models, Theoretical
  • Pandemics

Substances

  • Autoantibodies
  • Autoantigens
  • Cytokines