Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the current COVID-19 pandemic, has caused more than 4.5 million deaths worldwide. Severe and fatal cases of COVID-19 are often associated with increased proinflammatory cytokine levels including interleukin 6 (IL-6) and acute respiratory distress syndrome. In this study, we explored the feasibility of using plants to produce an anti-IL-6 receptor (IL-6R) monoclonal antibody (mAb) and examined its utility in reducing IL-6 signaling in an in vitro model, which simulates IL-6 induction during SARS-CoV-2 infection. The anti-IL6R mAb (IL6RmAb) was quickly expressed and correctly assembled in Nicotiana benthamiana leaves. Plant-produced IL6RmAb (pIL6RmAb) could be enriched to homogeneity by a simple purification scheme. Furthermore, pIL6RmAb was shown to effectively inhibit IL-6 signaling in a cell-based model system. Notably, pIL6RmAb also suppressed IL-6 signaling that was induced by the exposure of human peripheral blood mononuclear cells to the spike protein of SARS-CoV-2. This is the first report of a plant-made anti-IL-6R mAb and its activity against SARS-CoV-2-related cytokine signaling. This study demonstrates the capacity of plants for producing functionally active mAbs that block cytokine signaling and implies their potential efficacy to curb cytokine storm in COVID-19 patients.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19) and has infected over 220 million people, causing more than 5.1 million deaths globally since its emergence [1]
Expression and Characterization of IL6R monoclonal antibodies (mAbs) (IL6RmAb) Produced in N. benthamiana
The IL6RmAb expressed in N. benthamiana plants and assembled correctly compared to that was of noquickly treatment negative control
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19) and has infected over 220 million people, causing more than 5.1 million deaths globally since its emergence [1]. A characteristic seen in severe cases of COVID-19 appears to be a dysregulated immune response, resulting in cytokine storm and immunopathology [4]. This indicates that systemic inflammation is correlated with more severe states of disease [4]. It has been shown that SARS-CoV-2 spike (S) and nucleocapsid proteins alone can induce production of IL-6 in monocytes and macrophages, and such IL-6 upregulation may be a trigger that initiates the dysregulated immune response in some COVID-19 patients [7]
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