Abstract

Coronaviruses belonging to the Coronaviridae family are single-stranded RNA viruses. The entry of SARS-CoV-2 is accomplished via ACE-2 receptors. SARS-CoV-2 infection coactivates both innate and adaptive immune responses. Although SARS-CoV-2 stimulates antibody production with a typical pattern of IgM/IgG, cellular immunity is also impaired. In severe cases, low CD4 + and CD8 + T cell counts are associated with impaired immune functions, and high neutrophil/lymphocyte ratios accompanying low lymphocyte subsets have been demonstrated. Recently, high IFN -α/γ ratios with impaired T cell responses, and increased IL-1, IL-6, TNF-α, MCP-1, IP-10, IL-4, IL-10 have been reported in COVID-19 infection. Increased proinflammatory cytokines and chemokines in patients with severe COVID-19 may cause the suppression of CD4 + and CD8 + T cells and regulatory T cells, causing excessive inflammatory responses and fatal cytokine storm with tissue and organ damage. Consequently, novel therapeutics to be developed against host immune system, including blockade of cytokines (IL-6, IL-1, IFN) themselves, their receptors or signaling pathways- JAK inhibitors- could be effective as potential therapeutics.

摘要

属于冠状病毒科的冠状病毒是单链 RNA 病毒。SARS-CoV-2 的进入是通过 ACE-2 受体完成的。SARS-CoV-2 感染共同激活先天性和适应性免疫反应。尽管 SARS-CoV-2 以典型的 IgM/IgG 模式刺激抗体产生，但细胞免疫也会受损。在严重的情况下，低 CD4 + 和 CD8 + T 细胞计数与免疫功能受损有关，并且已经证明伴随低淋巴细胞亚群的高中性粒细胞/淋巴细胞比率。最近，在 COVID-19 中报道了高 IFN-α/γ 比率与受损的 T 细胞反应，以及增加的 IL-1、IL-6、TNF-α、MCP-1、IP-10、IL-4、IL-10。 19 感染。重症COVID-19患者体内促炎细胞因子和趋化因子的增加可能会导致CD4+和CD8+T细胞和调节性T细胞受到抑制，导致过度的炎症反应和致命的细胞因子风暴，并伴有组织和器官损伤。因此，针对宿主免疫系统开发的新疗法，包括阻断细胞因子（IL-6、IL-1、IFN）本身、它们的受体或信号通路——JAK 抑制剂——可能是有效的潜在疗法。