Elsevier

Clinical Immunology

Volume 217, August 2020, 108487
Clinical Immunology

Letter to the Editor
Type 3 hypersensitivity in COVID-19 vasculitis

https://doi.org/10.1016/j.clim.2020.108487Get rights and content

Highlights

  • COVID-19 is an ongoing public health emergency around the world.

  • New knowledge about its immunopathogenic mechanisms is required.

  • Type 3 hypersensitivity reaction in COVID-19 vasculitis is here disclosed.

  • Inflamed vascular smooth muscle cells concur to the cytokine storm via IL-6.

  • Histology, histochemistry and immunofluorescence have been successfully applied.

Abstract

Coronavirus Disease 2019 (COVID-19) is an ongoing public health emergency and new knowledge about its immunopathogenic mechanisms is deemed necessary in the attempt to reduce the death burden, globally. For the first time in worldwide literature, we provide scientific evidence that in COVID-19 vasculitis a life-threatening escalation from type 2 T-helper immune response (humoral immunity) to type 3 hypersensitivity (immune complex disease) takes place. The subsequent deposition of immune complexes inside the vascular walls is supposed to induce a severe inflammatory state and a cytokine release syndrome, whose interleukin-6 is the key myokine, from the smooth muscle cells of blood vessels.

Keywords

Coronavirus disease 2019 (COVID-19)
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)
Type III hypersensitivity
Immune complex disease
Vasculitis
Interleukin-6 (IL-6)

Cited by (0)

View Abstract