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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Macrophage receptor SR-AI is crucial to maintain normal plasma levels of coagulation factor X
Vincent Muczynski1, Amine Bazaa1, Cécile Loubière1
1Unité 1176 INSERM, Le Kremlin-Bicêtre, France; and Unité Mixte de Recherche S1176, Université Paris-Sud, Le Kremlin-Bicêtre, France.
Abstract:
Beside its classical role in the coagulation cascade, coagulation factor X (FX) is involved in several major biological processes including inflammation and enhancement of virus-induced immune responses. We recently reported that the long circulatory half-life of FX is linked to its interaction with liver-resident macrophages. Importantly, we now observed that macrophages, but not undifferentiated monocytes, support this interaction. Using cell biology approaches with primary and THP1-derived macrophages as well as transfected cells, we further identified the scavenger receptor type A member I (SR-AI) to be a macrophage-specific receptor for FX. This result was confirmed using SR-AI-deficient mice, which exhibit reduced circulating levels of FX in vivo and loss of FX-macrophage interactions in vitro. Binding studies using purified proteins revealed that FX binds specifically (half-maximal binding, 3 μg/mL) to the extracellular domain of SR-AI. Altogether, we demonstrate that macrophages regulate FX plasma levels in an SR-AI-dependent manner.
Insights
Macrophages regulate coagulation factor X (FX) levels through scavenger receptor type A member I (SR-AI). This interaction, specific to macrophages, impacts FX
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- Coagulation Factor X (FX) plays roles beyond coagulation, including in inflammation and immune responses.
- FX's long circulatory half-life is associated with its interaction with liver-resident macrophages.
- This interaction is specific to differentiated macrophages, not monocytes.
Purpose of the Study:
- To identify the specific receptor on macrophages responsible for interacting with FX.
- To elucidate the mechanism by which macrophages regulate FX plasma levels.
Main Methods:
- Cell biology techniques using primary and THP1-derived macrophages.
- Studies with transfected cells and scavenger receptor type A member I (SR-AI)-deficient mice.
- Protein binding assays to quantify FX and SR-AI interaction.
Main Results:
- Scavenger receptor type A member I (SR-AI) was identified as a macrophage-specific receptor for FX.
- SR-AI-deficient mice showed reduced circulating FX levels and impaired FX-macrophage interaction.
- FX specifically binds to the extracellular domain of SR-AI with a half-maximal binding concentration of 3 μg/mL.
Conclusions:
- Macrophages regulate FX plasma levels in an SR-AI-dependent manner.
- SR-AI is crucial for FX-macrophage interactions and influences FX circulatory levels.
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