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
- ,
- ,
- ,
- 巻
- 499
- 号
- 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
- ID情報
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- DOI : 10.1016/j.bbrc.2018.04.035
- ISSN : 1090-2104
- ISSN : 0006-291X
- PubMed ID : 29627569
- SCOPUS ID : 85045112996