| First Author | Kurche JS | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 2 | Pages | 585-93 |
| PubMed ID | 22156349 | Mgi Jnum | J:180881 |
| Mgi Id | MGI:5308129 | Doi | 10.4049/jimmunol.1102550 |
| Citation | Kurche JS, et al. (2012) Type I IFN-dependent T cell activation is mediated by IFN-dependent dendritic cell OX40 ligand expression and is independent of T cell IFNR expression. J Immunol 188(2):585-93 |
| abstractText | Type I IFNs are important for direct control of viral infection and generation of adaptive immune responses. Recently, direct stimulation of CD4(+) T cells via type I IFNR has been shown to be necessary for the formation of functional CD4(+) T cell responses. In contrast, we find that CD4(+) T cells do not require intrinsic type I IFN signals in response to combined TLR/anti-CD40 vaccination. Rather, the CD4 response is dependent on the expression of type I IFNR (IFNalphaR) on innate cells. Further, we find that dendritic cell (DC) expression of the TNF superfamily member OX40 ligand was dependent on type I IFN signaling in the DC, resulting in a reduced CD4(+) T cell response that could be substantially rescued by an agonistic Ab to the receptor OX40. Taken together, we show that the IFNalphaR dependence of the CD4(+) T cell response is accounted for exclusively by defects in DC activation. |
