AI Article Synopsis
- SLAMF1 is an immune receptor that helps activate signaling pathways in immune cells, essential for their function.
- This study highlights SLAMF1's role in enabling TLR4 to induce interferon β and enhance the ability of human macrophages to kill Gram-negative bacteria.
- The research also reveals that SLAMF1 assists in moving TRAM to the phagosomes where bacteria are attacked, suggesting it could be a target for controlling inflammatory responses in humans.
Article Abstract
Signaling lymphocytic activation molecule family 1 (SLAMF1) is an Ig-like receptor and a costimulatory molecule that initiates signal transduction networks in a variety of immune cells. In this study, we report that SLAMF1 is required for Toll-like receptor 4 (TLR4)-mediated induction of interferon β (IFNβ) and for killing of Gram-negative bacteria by human macrophages. We found that SLAMF1 controls trafficking of the Toll receptor-associated molecule (TRAM) from the endocytic recycling compartment (ERC) to phagosomes. In resting macrophages, SLAMF1 is localized to ERC, but upon addition of , it is trafficked together with TRAM from ERC to phagosomes in a Rab11-dependent manner. We found that endogenous SLAMF1 protein interacted with TRAM and defined key interaction domains as amino acids 68 to 95 of TRAM as well as 15 C-terminal amino acids of SLAMF1. Interestingly, the SLAMF1-TRAM interaction was observed for human but not mouse proteins. Overall, our observations suggest that SLAMF1 is a new target for modulation of TLR4-TRAM-TRIF inflammatory signaling in human cells.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5881497 | PMC |
| http://dx.doi.org/10.1083/jcb.201707027 | DOI Listing |
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