Institute of Pathology, University of Modena and Reggio Emilia, Modena, Italy; Hemolymphopathology Team, University Hospital of Modena, Modena, Italy; Immunohistochemistry Lab, University Hospital of Modena, Modena, Italy.
Nephrology Lab, University of Modena and Reggio Emilia, Modena, Italy.
Clin Immunol. 2020 Aug;217:108487. doi: 10.1016/j.clim.2020.108487. Epub 2020 May 29.
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.
2019 年冠状病毒病（COVID-19）是一场持续的公共卫生紧急事件，为了降低全球死亡负担，人们认为有必要了解其免疫发病机制的新认识。我们首次在世界范围内的文献中提供科学证据，表明 COVID-19 血管炎从 2 型辅助性 T 细胞免疫反应（体液免疫）发展为 3 型超敏反应（免疫复合物病）是一种危及生命的升级过程。随后免疫复合物在血管壁内的沉积，据推测会引起严重的炎症状态和细胞因子释放综合征，其白介素-6 是血管平滑肌细胞的关键肌细胞因子。
