Abstract
Toll-like receptors (TLRs) expressed on antigen-presenting cells (APCs), form a critical link between innate and the adaptive immune responses. Activation of TLRs by LPS and dsRNA results in up-regulation of co-stimulatory molecules (UCM) essential for the generation of robust T-cell responses. It is now evident that type I interferons (IFNs) play an important role in UCM and in the subsequent maturation of APCs. The recently identified adaptor molecules Trif and Tram, unlike their counterparts MyD88 and MAL/Tirap, induce type I IFN via the TLR4 signaling pathway, whereas Trif appears to be the sole adaptor molecule involved in TLR3 signaling, resulting in subsequent production of type I IFN. Here, we discuss how Trif and type I IFN are involved in the optimization of APC-T cell interaction in response not only to viral but also bacterial stimuli.
Original language | English (US) |
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Pages (from-to) | 130-136 |
Number of pages | 7 |
Journal | Journal of Endotoxin Research |
Volume | 10 |
Issue number | 2 |
DOIs | |
State | Published - 2004 |
Keywords
- Adaptive immune responses
- Interferon
- Tram
- Trif
ASJC Scopus subject areas
- Microbiology
- Immunology
- Molecular Biology
- Cell Biology
- Infectious Diseases