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Human In Vitro Suppression as Screening Tool for the Recognition of an Early State of Immune Imbalance
Published on: July 22, 2011
Human monocyte-derived suppressive cells (HuMoSC) for cell therapy in giant cell arteritis
Maxime Samson1,2,3, Coraline Genet2, Marc Corbera-Bellalta3
1Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, Dijon, France.
Insights
Human Monocyte-derived Suppressor Cells (HuMoSC) show potential in treating Giant Cell Arteritis (GCA) by reducing vascular inflammation and remodeling. This novel cell therapy offers a promising new avenue for GCA management.
Area of Science:
- Immunology
- Vascular Biology
- Regenerative Medicine
Background:
- Giant Cell Arteritis (GCA) pathogenesis involves vascular inflammation and remodeling.
- Current GCA treatments inadequately address vascular remodeling, representing an unmet clinical need.
Purpose of the Study:
- To investigate the therapeutic potential of Human Monocyte-derived Suppressor Cells (HuMoSC) in mitigating vascular inflammation and remodeling in GCA.
- To evaluate the impact of HuMoSCs and their supernatant on key molecular pathways involved in GCA pathogenesis.
Main Methods:
- Temporal artery fragments from GCA patients were cultured with or without HuMoSCs or their supernatant.
- Gene expression (mRNA) in arterial tissue and protein concentrations in culture supernatant were analyzed.
- Vascular smooth muscle cell (VSMC) proliferation and migration were assessed in response to PDGF and HuMoSC supernatant.
Main Results:
- HuMoSCs significantly decreased transcripts and proteins associated with vascular inflammation (e.g., CCL2, CCR2) and remodeling (e.g., PDGF, VEGF).
- HuMoSC supernatant inhibited PDGF-induced VSMC proliferation and migration, potentially via mTOR pathway inhibition.
- HuMoSC recruitment into the arterial wall was mediated by CCR5 signaling.
Conclusions:
- HuMoSCs and their supernatant demonstrate efficacy in reducing vascular inflammation and remodeling in GCA.
- This cell therapy represents a promising approach to address the unmet need for improved GCA treatment, particularly for vascular remodeling.
Introduction:
The pathogenesis of Giant Cell Arteritis (GCA) relies on vascular inflammation and vascular remodeling, the latter being poorly controlled by current treatments.
Methods:
This study aimed to evaluate the effect of a novel cell therapy, Human Monocyte-derived Suppressor Cells (HuMoSC), on inflammation and vascular remodeling to improve GCA treatment. Fragments of temporal arteries (TAs) from GCA patients were cultured alone or in the presence of HuMoSCs or their supernatant. After five days, mRNA expression was measured in the TAs and proteins were measured in culture supernatant. The proliferation and migration capacity of vascular smooth muscle cells (VSMCs) were also analyzed with or without HuMoSC supernatant.
Results:
Transcripts of genes implicated in vascular inflammation (CCL2, CCR2, CXCR3, HLADR), vascular remodeling (PDGF, PDGFR), angiogenesis (VEGF) and extracellular matrix composition (COL1A1, COL3A1 and FN1) were decreased in arteries treated with HuMoSCs or their supernatant. Likewise, concentrations of collagen-1 and VEGF were lower in the supernatants of TAs cultivated with HuMoSCs. In the presence of PDGF, the proliferation and migration of VSMCs were both decreased after treatment with HuMoSC supernatant. Study of the PDGF pathway suggests that HuMoSCs act through inhibition of mTOR activity. Finally, we show that HuMoSCs could be recruited in the arterial wall through the implication of CCR5 and its ligands.
Conclusion:
Altogether, our results suggest that HuMoSCs or their supernatant could be useful to decrease vascular in flammation and remodeling in GCA, the latter being an unmet need in GCA treatment.
