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H2‐D d ‐mediated upregulation of interleukin‐4 production by natural killer T‐cell and dendritic cell interaction
Author(s) -
Mizuuchi Kazuomi,
Yanagawa Yoshiki,
Iwabuchi Kazuya,
Namba Kenichi,
Kitaichi Nobuyoshi,
Ohno Shigeaki,
Onoé Kazunori
Publication year - 2008
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2007.02744.x
Subject(s) - natural killer t cell , tlr9 , cpg site , dendritic cell , microbiology and biotechnology , biology , immune system , cpg oligodeoxynucleotide , downregulation and upregulation , cytokine , immunology , t cell , interleukin 12 , interleukin 15 , receptor , cytotoxic t cell , interleukin , dna methylation , biochemistry , gene expression , gene , in vitro
Summary Natural killer T (NKT) cells are capable of subserving apparently opposite functions, the interferon‐γ (IFN‐γ)‐mediated enhancement of host defence and interleukin‐4 (IL‐4) ‐mediated immune regulation. Although dendritic cells (DCs) potently activate NKT cells, DC regulation of the IL‐4–IFN‐γ balance via NKT‐cell activation is not well characterized. In the present study, we examined the effect of DC treatment with CpG oligodeoxynucleotide (ODN), a Toll‐like receptor 9 ligand, on the induction of NKT‐cell cytokine production. CpG‐ODN‐conditioned and α‐galactosylceramide (α‐GalCer)‐loaded myeloid DCs (CpG‐DCs) from BALB/c mice showed enhanced ability to induce NKT‐cell production of IL‐4, but not IFN‐γ, compared to α‐GalCer‐loaded control DCs (not treated with CpG‐ODN). The CpG‐DCs expressed significantly higher levels of H2‐D d than control DCs, and blocking of the H2‐D d and Ly49 receptor interaction during antigen presentation completely abolished the enhanced ability of the CpG‐DCs to induce NKT‐cell production of IL‐4. These findings demonstrate that DC recognition of the CpG motif leads to induction of enhanced IL‐4 production by NKT cells via interaction of the augmented H2‐D d with Ly49 receptors on NKT cells.