CCL2, but not its receptor, is essential to restrict immune privileged central nervous system‐invasion of Japanese encephalitis virus via regulating accumulation of CD11b(+) Ly‐6C(hi) monocytes

Lignende værker

• Exacerbation of Japanese Encephalitis by CD11c(hi) Dendritic Cell Ablation Is Associated with an Imbalance in Regulatory Foxp3(+) and IL-17(+)CD4(+) Th17 Cells and in Ly-6C(hi) and Ly-6C(lo) Monocytes
  af: Choi, Jin Young, et al.
  Udgivet: (2017)
• Distinct Upstream Role of Type I IFN Signaling in Hematopoietic Stem Cell-Derived and Epithelial Resident Cells for Concerted Recruitment of Ly-6C(hi) Monocytes and NK Cells via CCL2-CCL3 Cascade
  af: Uyangaa, Erdenebileg, et al.
  Udgivet: (2015)
• CD11c(hi) Dendritic Cells Regulate Ly-6C(hi) Monocyte Differentiation to Preserve Immune-privileged CNS in Lethal Neuroinflammation
  af: Kim, Jin Hyoung, et al.
  Udgivet: (2015)
• Amelioration of Japanese encephalitis by blockage of 4-1BB signaling is coupled to divergent enhancement of type I/II IFN responses and Ly-6C(hi) monocyte differentiation
  af: Kim, Seong Bum, et al.
  Udgivet: (2015)
• Blockage of indoleamine 2,3-dioxygenase regulates Japanese encephalitis via enhancement of type I/II IFN innate and adaptive T-cell responses
  af: Kim, Seong Bum, et al.
  Udgivet: (2016)