AI Article Synopsis
- TLR4 is important for fighting infections but can cause inflammation if its signaling goes awry.
- Antibodies that block the CXCR4 receptor lead to heightened TLR4 signaling, indicating CXCR4's role in regulating TLR4.
- Enhancing CXCR4 expression or adding its ligand SDF-1 decreases TLR4 activity, hinting at potential new treatments for conditions related to TLR4 overactivity.
Article Abstract
The response of Toll-like receptor 4 (TLR4) to lipopolysaccharide (LPS) is thought vital for resisting infection. Since aberrant TLR4 signaling may initiate inflammatory conditions such as the sepsis syndrome, we sought a component of normal cells that might provide local control of TLR4 activation. We found that antibodies that block chemokine receptor 4 (CXCR4) function enhanced TLR4 signaling, while increased expression of CXCR4 or addition of the CXCR4 ligand SDF-1 suppressed TLR4 signaling induced by LPS. These findings suggest that CXCR4 could exert local control of TLR4 and suggest the possibility of new therapeutic approaches to suppression of TLR4 function.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.febslet.2004.12.047 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!