論文

査読有り 筆頭著者 責任著者 国際誌
2018年5月23日

TICAM-1 is dispensable in STING-mediated innate immune responses in myeloid immune cells.

Biochemical and biophysical research communications
  • Ken Takashima
  • ,
  • Hiroyuki Oshiumi
  • ,
  • Misako Matsumoto
  • ,
  • Tsukasa Seya

499
4
開始ページ
985
終了ページ
991
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2018.04.035
出版者・発行元
Elsevier B.V.

Stimulator of interferon genes (STING) is an essential molecule for the production of type I interferon (IFN), and other inflammatory cytokines, in response to cytosolic DNA. STING contributes to host defense against infection and anti-tumor responses. Previous reports have demonstrated that STING signaling is required by the adaptor Toll-IL-1 receptor-containing adaptor molecule-1 (TICAM-1), which has been identified as a TLR3-adaptor molecule using mouse embryonic fibroblasts. Here, we demonstrate that TICAM-1 does not affect STING-mediated innate immune responses, as increases in the mRNA expression levels of IFN-β, IL-6, and CCL5 were observed in bone marrow-derived or splenic myeloid cells. Moreover, STING ligand-enhanced co-stimulatory molecule expression, including CD80, CD86, and CD40, was detected on splenic CD11c + DCs, even in Ticam-1-deficient mice. Our results suggest that STING-mediated innate immune responses and dendritic cell maturation do not require TICAM-1 in myeloid lineage immune cells. TICAM-1 is ubiquitously expressed, even in cell types which do not express TLR3. Therefore, TICAM-1 may possess different functions depending on cell type and signaling purposes.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2018.04.035
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/29627569
ID情報
  • DOI : 10.1016/j.bbrc.2018.04.035
  • ISSN : 1090-2104
  • ISSN : 0006-291X
  • PubMed ID : 29627569
  • SCOPUS ID : 85045112996

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