期刊
JOURNAL OF IMMUNOLOGY
卷 188, 期 2, 页码 585-593出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1102550
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资金
- National Institutes of Health [AI06877, AI066121]
- Department of Defense [W81XWH-07-1-0550]
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 (IFN alpha R) 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 IFN alpha R dependence of the CD4(+) T cell response is accounted for exclusively by defects in DC activation. The Journal of Immunology, 2012, 188: 585-593.
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