Abstract：
COVID-19, caused by the SARS-CoV-2 virus, has caused a global health crisis, necessitating a deeper understanding of its pathophysiology. In this study, we explored the immune and hematological dynamics in COVID-19 patients to gain insights into disease severity and prognosis. Our findings revealed distinct cytokine profiles in moderate and severe cases. IL12A was significantly upregulated in peripheral blood mononuclear cells from moderate cases, suggesting a potential role in initiating an effective immune response. Conversely, severe cases exhibited downregulation of key pro-inflammatory cytokines (IL23A, TNFalpha, IL1B, and IFNG) alongside an upregulation of the immunosuppressive IL10, indicative of a dysregulated immune environment. Serum analysis showed elevated IL6 and IL10 levels in both moderate and severe cases, emphasizing their potential as markers for disease severity. Notably, no significant differences in serum cytokines were found between recovery and lethal cases. In lethal cases of COVID-19, elevated D-dimer, urea, and creatinine correlated with IL6 and IL10. This study contributes valuable information to the ongoing efforts to understand and manage the dysregulated immune responses underlying COVID-19 pathology.
摘要：
由SARS-CoV-2病毒引起的COVID-19，引发了全球健康危机，需要对其病理生理学有更深入的了解。在这项研究中,我们探索了COVID-19患者的免疫和血液学动力学，以了解疾病的严重程度和预后。我们的发现揭示了中度和重度病例中不同的细胞因子谱。IL12A在中度病例的外周血单核细胞中显著上调，提示在启动有效的免疫反应中的潜在作用。相反，严重病例表现出关键促炎细胞因子的下调(IL23A，TNFα,IL1B,和IFNG）以及免疫抑制性IL10的上调，表明免疫环境失调。血清分析显示，在中度和重度病例中IL6和IL10水平均升高，强调它们作为疾病严重程度标志的潜力。值得注意的是,在恢复和致死病例之间，血清细胞因子没有显着差异。在COVID-19的致死病例中，D-二聚体升高，尿素,肌酐与IL6和IL10相关。这项研究为正在进行的了解和管理COVID-19病理学基础上的失调免疫反应的努力提供了有价值的信息。
