Abstract
Both lipopolysaccharide (LPS) and double-stranded RNA (dsRNA) are adjuvants for the adaptive immune response, inducing upregulation of costimulatory molecules (UCM) on antigen-presenting cells. Trif, an adapter protein that transduces signals from Toll-like receptor 4 (TLR4) and TLR3, permits the induction of many cytokines, including interferon-β, which signals through the type I interferon receptor. We show here that LPS-induced UCM was strictly dependent on the TLR4→Trif axis, whereas dsRNA-induced UCM was only partly dependent on the TLR3→Trif axis. But both LPS-and dsRNA-induced UCM were entirely dependent on type I interferon receptor signaling. These findings show that UCM involves an autocrine or paracrine loop, and indicate that an alternative TLR3-independent, Trif-independent pathway contributes to dsRNA-induced UCM.
Original language | English (US) |
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Pages (from-to) | 1223-1229 |
Number of pages | 7 |
Journal | Nature immunology |
Volume | 4 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2003 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology