| First Author | Park HJ | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 396 |
| Issue | 3 | Pages | 721-5 |
| PubMed ID | 20450885 | Mgi Jnum | J:162501 |
| Mgi Id | MGI:4819064 | Doi | 10.1016/j.bbrc.2010.04.169 |
| Citation | Park HJ, et al. (2010) TLR4-mediated activation of mouse macrophages by Korean mistletoe lectin-C (KML-C). Biochem Biophys Res Commun 396(3):721-5 |
| abstractText | Korean mistletoe lectin (KML-C) is an adjuvant that activates systemic and mucosal immune cells to release cytokines including TNF-alpha, which induces immunity against viruses and cancer cells. Although the immunomodulatory activity of KML-C has been well established, the underlying mechanism of action of KML-C has yet to be explored. When mouse peritoneal macrophages were treated with KML-C, both transcription and translation of TLR4 were upregulated. KML-C-induced TLR4 downstream events were similar to those activated by LPS: the upregulation of interleukin-1 receptor-associated kinase-1 (IRAK1); resulting in macrophage activation and TNF-alpha production. When TLR4 was blocked using a TLR4-specific neutralizing antibody, TNF-alpha production from the macrophages was significantly inhibited. Moreover, TLR4-deficient mouse macrophages treated with KML-C also secreted greatly reduced level of TNF-alpha secretion. Finally, TLR4 molecules were co-precipitated with KML-C, to which agarose beads were conjugated, indicating that those molecules are associated. These data indicate that KML-C activates mouse macrophages to secrete TNF-alpha by interacting with the TLR4 molecule and activating its signaling pathways. |
