6 Matching Annotations
  1. Jun 2020
    1. Long, Q.-X., Tang, X.-J., Shi, Q.-L., Li, Q., Deng, H.-J., Yuan, J., Hu, J.-L., Xu, W., Zhang, Y., Lv, F.-J., Su, K., Zhang, F., Gong, J., Wu, B., Liu, X.-M., Li, J.-J., Qiu, J.-F., Chen, J., & Huang, A.-L. (2020). Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections. Nature Medicine, 1–5. https://doi.org/10.1038/s41591-020-0965-6

  2. Apr 2020
    1. In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.
    1. Third, Huang’s study noted that high concentration of IL-1β, IFN-γ, IP-10 and MCP-1 could be detected in patients infected with 2019-nCoV, which might lead to activated T-helper-1 (Th1) cell responses [4]. Furthermore, they also found that ICU patients had much higher concentrations of inflammatory factors than those non-ICU patients, suggesting that the cytokine storm was associated with disease severity
    1. Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells
  3. Oct 2017
    1. Upon synapse formation, T cells not only release perforin and granzyme B but also release large amounts of cytokines, namely interleukin (IL)-6, IL-10, and interferon (IFN)-γ