Presently, we need more therapeutic molecules for this COVID-19 outbreak. The severity and mortality of the disease is associated with a high level of release of cytokine in the patients which is known as CRS (cytokine release syndrome) or cytokine storm syndrome. IL-6 is a type of pro-inflammatory cytokine which release in the severe COVID-19 patients. This cytokine initiates CRS the JAK-STAT or MAPK/NF-κB-IL-6 pathway. Tocilizumab, a humanized monoclonal antibody, is designed to bind both mIL-6R (membrane bound receptor for IL-6) and sIL-6R (soluble receptor for IL-6) and inhibit the JAK-STAT or MAPK/NF-κB-IL-6 signaling pathway. It finally stops the cytokine storm syndrome. However, we need to understand that how tocilizumab is bound with mIL-6R or sIL-6R. Similarly, we also need to understand more about the real molecular mechanism of activity of tocilizumab.

目前，我们需要更多的治疗分子来应对 COVID-19 的爆发。该疾病的严重性和死亡率与患者体内细胞因子的高水平释放有关，这被称为 CRS（细胞因子释放综合征）或细胞因子风暴综合征。IL-6 是一种促炎细胞因子，在重症 COVID-19 患者中释放。这种细胞因子通过 JAK-STAT 或 MAPK/NF-κB-IL-6 通路启动 CRS。Tocilizumab 是一种人源化单克隆抗体，旨在结合 mIL-6R（IL-6 膜结合受体）和 sIL-6R（IL-6 可溶性受体）并抑制 JAK-STAT 或 MAPK/NF-κB-IL -6 信号通路。它最终阻止了细胞因子风暴综合症。但是，我们需要了解tocilizumab 是如何与mIL-6R 或sIL-6R 结合的。相似地，