<p>Platelet transfusion is important in clinical treatment, especially for patients with hematological diseases. In this study, an in vitro transfusion model was established to explore the effects of apheresis platelets on the immune responses of myeloid dendritic cells (mDCs) and a specialized subset of DCs with blood DC antigen (BDCA3<sup>+</sup>). The results demonstrated that during viral infection simulation, exposure to apheresis platelets reduced CD83 expression on mDCs. However, no significant effect on the expression of surface antigens on BDCA3<sup>+</sup> DCs was observed when they were exposed to apheresis platelets. In addition, exposure did not affect the production of inflammatory mediators by either type of DC. Apheresis platelets can alter the overall leukocyte inflammatory response of recipients. The levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-8, and monocyte chemoattractant protein-1 (MCP-1) were increased upon exposure to apheresis platelets alone. In the simulation of viral infection, the levels of IL-8, MCP-1, IFN-γ and IL-12p70 were increased, and the IP-10 level was inhibited. In the bacterial infection simulation, the IL-8 and MCP-1 levels were increased, whereas the IL-10 and IP-10 levels were decreased. In conclusion, apheresis platelet transfusion may inhibit the maturation and activation of mDCs during viral infection and enhance the overall leukocyte inflammatory response in recipients.</p>

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Apheresis platelets modulate myeloid dendritic cell immune responses

  • Mengyuan Ding,
  • Yan Li,
  • Qi Xiao,
  • Mingyuan Wang,
  • Xiao Feng

摘要

Platelet transfusion is important in clinical treatment, especially for patients with hematological diseases. In this study, an in vitro transfusion model was established to explore the effects of apheresis platelets on the immune responses of myeloid dendritic cells (mDCs) and a specialized subset of DCs with blood DC antigen (BDCA3+). The results demonstrated that during viral infection simulation, exposure to apheresis platelets reduced CD83 expression on mDCs. However, no significant effect on the expression of surface antigens on BDCA3+ DCs was observed when they were exposed to apheresis platelets. In addition, exposure did not affect the production of inflammatory mediators by either type of DC. Apheresis platelets can alter the overall leukocyte inflammatory response of recipients. The levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-8, and monocyte chemoattractant protein-1 (MCP-1) were increased upon exposure to apheresis platelets alone. In the simulation of viral infection, the levels of IL-8, MCP-1, IFN-γ and IL-12p70 were increased, and the IP-10 level was inhibited. In the bacterial infection simulation, the IL-8 and MCP-1 levels were increased, whereas the IL-10 and IP-10 levels were decreased. In conclusion, apheresis platelet transfusion may inhibit the maturation and activation of mDCs during viral infection and enhance the overall leukocyte inflammatory response in recipients.