| First Author | Gupta S | Year | 2006 |
| Journal | Cell Immunol | Volume | 243 |
| Issue | 2 | Pages | 75-82 |
| PubMed ID | 17292338 | Mgi Jnum | J:120856 |
| Mgi Id | MGI:3708164 | Doi | 10.1016/j.cellimm.2006.12.004 |
| Citation | Gupta S, et al. (2006) CpG-induced IFNgamma expands TLR4-specific IL-18 responses in vivo. Cell Immunol 243(2):75-82 |
| abstractText | Serum IL-18 responses to LPS increase after pretreatment with CpG-containing DNA. Compared to saline-pretreated controls, mice pretreated with CpG for two days produced 20-fold more serum IL-18 when challenged with lipopolysaccharide (LPS). In contrast, IFNgamma-deficiency or anti-IFNgamma pretreatment reduced CpG-expanded IL-18 responses to LPS by 67 and 83%, respectively. Mice pretreated with either IFNgamma or CpG comparably increased LPS-inducible serum IL-18 responses. LPS, compared to challenge with other TLR agonists, was best able to trigger high serum IL-18 levels in CpG-pretreated mice and this response was TLR4-dependent. CpG, compared to pretreatment with other TLR agonists, optimally expanded LPS-induced IL-18 responses that correlated with higher levels of circulating IFNgamma levels prior to LPS challenge. High-level serum IL-18 responses were caspase-1-dependent and P2X7 receptor-independent. We conclude that CpG promotes high-level IL-18 synthesis by an IFNgamma-dependent and IFNgamma-sufficient mechanism in vivo that is optimally triggered by LPS. |
