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Breast cancer-induced immune suppression in the sentinel lymph node is effectively countered by CpG-B in conjunction with inhibition of the JAK2/STAT3 pathway.

Kim M van PulRonald J C L M VuylstekeMonique T A de BeijerRieneke van de VenM Petrousjka van den TolHein B A C StockmannTanja D de Gruijl
Published in: Journal for immunotherapy of cancer (2021)
Ex vivo immune modulation of the SLN by CpG-B and simultaneous JAK2/STAT3 inhibition can effectively overcome BrC-induced immune suppression by preferential activation of LNR DC, ultimately restoring type 1-mediated antitumor immunity, thereby securing a BrC-specific T cell response. These findings provide a clear rationale for clinical exploration of SLN-immune potentiation through local CpG/STAT3i administration in patients with BrC.
Keyphrases
  • sentinel lymph node
  • dna methylation
  • high glucose
  • lymph node
  • early stage
  • diabetic rats
  • drug induced
  • dendritic cells
  • gene expression
  • squamous cell carcinoma
  • young adults
  • endothelial cells