Department of Biotechnology, School of Life Science and Biotechnology, Adamas University, Kolkata, West Bengal, India.
Institute for Skeletal Aging and Orthopedic Surgery, Hallym University-Chuncheon Sacred Heart Hospital, Chuncheon-si, Gangwon-do, South Korea.
Arch Med Res. 2020 Aug;51(6):595-597. doi: 10.1016/j.arcmed.2020.05.009. Epub 2020 May 21.
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,我们需要更多针对这种 COVID-19 爆发的治疗性分子。这种疾病的严重程度和死亡率与患者体内高水平的细胞因子释放有关,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,在严重的 COVID-19 患者中释放。这种细胞因子引发 CRS,即 JAK-STAT 或 MAPK/NF-κB-IL-6 途径。托珠单抗是一种人源化单克隆抗体,旨在结合 mIL-6R(IL-6 的膜结合受体)和 sIL-6R(IL-6 的可溶性受体),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征。然而,我们需要了解托珠单抗如何与 mIL-6R 或 sIL-6R 结合。同样,我们也需要更多地了解托珠单抗的实际分子作用机制。
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