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Wnt5a inhibits the CpG oligodeoxynucleotide‐triggered activation of human plasmacytoid dendritic cells
Author(s) -
Hack K.,
Reilly L.,
Proby C.,
Fleming C.,
Leigh I.,
Foerster J.
Publication year - 2012
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/j.1365-2230.2012.04362.x
Subject(s) - cd86 , secretion , wnt5a , cd80 , cpg oligodeoxynucleotide , plasmacytoid dendritic cell , cpg site , immunology , melanoma , immune system , cancer research , biology , interferon , immunity , cancer immunotherapy , downregulation and upregulation , microbiology and biotechnology , dendritic cell , immunotherapy , wnt signaling pathway , cd40 , signal transduction , t cell , gene , cytotoxic t cell , in vitro , gene expression , genetics , dna methylation , endocrinology
Summary Plasmacytoid dendritic cells (pDCs) fulfil multiple roles in immunity, and can secrete large amounts of interferon (IFN)‐α. However, the available evidence suggests that they may actually counteract efficient antitumour immunity. Thus in melanoma, pDCs are abundant, but they are anergic and deficient in IFN‐α secretion. pDC anergy is thought to be caused by immunosuppressive factors secreted by melanoma cells. One factor strongly expressed by melanoma is Wnt5a, which is implicated in cancer tissue invasion. In this paper, we show that Wnt5a is able to block the upregulation of the activation markers CD80 and CD86 on naive human pDCs stimulated by CpG oligodeoxynucleotide, and CpG‐triggered secretion of IFN‐α by pDCs. Our results suggest that Wnt5a may not only initiate cancer invasion, but could also regulate activation of pDC. These data provide a clear rationale to investigate a role for Wnt5a in immune regulation.