| First Author | Takashima K | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 499 |
| Issue | 4 | Pages | 985-991 |
| PubMed ID | 29627569 | Mgi Jnum | J:272473 |
| Mgi Id | MGI:6280398 | Doi | 10.1016/j.bbrc.2018.04.035 |
| Citation | Takashima K, et al. (2018) TICAM-1 is dispensable in STING-mediated innate immune responses in myeloid immune cells. Biochem Biophys Res Commun 499(4):985-991 |
| abstractText | 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-beta, 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. |
