AI Article Synopsis
- Patrolling Ly6C(-) monocytes are important immune cells involved in inflammation and pathogen defense, and they express high levels of the receptor S1PR5, similar to NK cells.
- The study found that mice lacking S1PR5 (S1pr5(-/-) mice) have no Ly6C(-) monocytes in their bloodstream but have normal amounts in the bone marrow, indicating S1PR5 is crucial for their exit from the bone marrow.
- Interestingly, the research showed that S1P (the ligand for S1PR5) does not attract these monocytes or affect their survival in lab conditions, suggesting S1PR5 plays a role in monocyte movement that is not dependent on S1P signaling
Article Abstract
Patrolling Ly6C(-) monocytes are blood-circulating cells that play a role in inflammation and in the defense against pathogens. Here, we show that similar to natural killer (NK) cells, patrolling monocytes express high levels of S1PR5, a G-coupled receptor for sphingosine-1 phosphate. We found that S1pr5(-/-) mice lack peripheral Ly6C(-) monocytes but have a normal number of these cells in the bone marrow (BM). Various lines of evidence exclude a direct contribution of S1PR5 in the survival of Ly6C(-) monocytes at the periphery. Rather, our data support a role for S1PR5 in the egress of Ly6C(-) monocytes from the BM. In particular, we observed a reduced frequency of patrolling monocytes in BM sinusoids of S1PR5 KO mice. Unexpectedly, S1P was not a chemoattractant for patrolling monocytes and had no significant effect on their viability in vitro. Moreover, the disruption of S1P gradients in vivo did not alter Ly6C(-) monocyte trafficking and viability. These data suggest that S1PR5 regulates the trafficking of monocytes via a mechanism independent of S1P gradients.
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| http://dx.doi.org/10.1002/eji.201343312 | DOI Listing |
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