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Neonatal Platelets Differentiate Monocytes to a Myeloid Derived Suppressor Cell Phenotype
Insights
Neonatal platelets, unlike adult platelets, promote monocytes to become immune-suppressing myeloid-derived suppressor cells (MDSCs). This finding suggests neonatal platelets may limit T-cell responses, impacting platelet transfusion outcomes in newborns.
Area of Science:
- Immunology
- Neonatal Biology
- Hematology
Background:
- Adult and neonatal platelets differ in immune molecule expression.
- Predicting platelet-immune cell interactions in neonates is complex due to varying factors.
- Previous studies showed adult platelet transfusion increased monocyte trafficking in neonatal mice.
Purpose of the Study:
- To investigate the immunomodulatory effects of neonatal versus adult platelets on monocytes.
- To determine if neonatal platelets induce a specific immune-suppressive phenotype in monocytes.
- To explore the mechanisms and in vivo relevance of these platelet-monocyte interactions.
Main Methods:
- Incubation of monocytes with neonatal or adult platelets and their releasates.
- Assessment of monocyte phenotype, including PD-L1 expression.
- Evaluation of T-cell activation in vitro and in vivo using an asthma-like model.
- Analysis of prostaglandin E2 (PGE2) and EP4 signaling pathways.
Main Results:
- Neonatal platelets, but not adult platelets, induced monocytes to adopt a myeloid-derived suppressor cell (MDSC) phenotype with increased PD-L1.
- Monocytes pre-incubated with neonatal platelets or releasates suppressed T-cell activation in vitro and in vivo.
- Neonatal platelet-induced monocyte suppression was mediated by increased PGE2 production signaling through monocyte EP4 receptors.
Conclusions:
- Neonatal platelets possess immune-limiting functions by indirectly suppressing T-cell responses via monocyte modulation.
- These findings suggest a potential mechanism contributing to adverse outcomes observed with neonatal platelet transfusions.
- Understanding these differences is crucial for optimizing neonatal care and transfusion strategies.
Abstract:
Adult platelets are relatively enriched in immune related molecules compared to neonatal platelets, but neonatal platelets express some growth factors and enzymes at comparatively higher levels. This makes a prediction of platelet-immune cell interaction outcomes in neonates a challenge, as they are likely dependent on the cell type and tissue environment at the time of injury or infection. Our past studies revealed that the transfusion of adult but not neonatal platelets into thrombocytopenic neonatal mice led to an acute increase in monocyte trafficking. We have now found that neonatal, but not adult platelets, induce monocytes to a Myeloid Derived Suppressor Cell (MDSC) phenotype, typified by increased PD-L1, that limits T-cell activation in vitro and in vivo . Monocytes prior incubated with neonatal, but not adult platelets, or platelet releasates, limited T-cell activation in vitro . Using an in vivo asthma-like model we also found that the treatment of mice with monocytes prior incubated with neonatal platelet releasates limited T-cell activation in a asthma-like model. Platelet-driven effects were dependent on neonatal platelets producing more PGE 2 that signaled through monocyte EP4. These studies indicate that neonatal platelets have immune limiting roles in the post-natal period by indirectly limiting T-cell responses, perhaps contributing to the adverse outcomes of platelet transfusions to neonates.
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