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Updated: May 2, 2026
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
α2-Antiplasmin is associated with macrophage activation and fibrin deposition in a macrophage activation syndrome
Yosuke Kanno1, Kinomi Toyama1, Haruna Shibata1
1Department of Molecular Pathology, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kodo Kyo-tanabe, Kyoto, Japan.
Abstract:
Macrophage activation syndrome (MAS) is a life-threatening condition, characterized by cytopenia, multi-organ dysfunction, and coagulopathy associated with excessive activation of macrophages. In this study, we investigated the roles of alpha2-antiplasmin (α2AP) in the progression of MAS using fulminant MAS mouse model induced by toll-like receptor-9 agonist (CpG) and D-(+)-galactosamine hydrochloride (DG). α2AP deficiency attenuated macrophage accumulation, liver injury, and fibrin deposition in the MAS model mice. Interferon-γ (IFN-γ) is associated with macrophage activation, including migration, and plays a pivotal role in MAS progression. α2AP enhanced the IFN-γ-induced migration, and tissue factor production. Additionally, we showed that fibrin-induced macrophage activation and tumor necrosis factor-α production. Moreover, the blockade of α2AP by neutralizing antibodies attenuated macrophage accumulation, liver injury, and fibrin deposition in the MAS model mice. These data suggest that α2AP may regulate IFN-γ-induced responses and be associated with macrophage activation and fibrin deposition in the MAS progression.
Insights
Alpha2-antiplasmin (α2AP) exacerbates macrophage activation syndrome (MAS) by promoting macrophage migration and fibrin deposition. Blocking α2AP in a mouse model reduced MAS severity, suggesting α2AP as a potential therapeutic target.
Area of Science:
- Immunology
- Hematology
- Pathophysiology
Background:
- Macrophage activation syndrome (MAS) is a severe, life-threatening hyperinflammatory condition.
- MAS involves excessive macrophage activation, leading to cytopenia, multi-organ dysfunction, and coagulopathy.
Purpose of the Study:
- To investigate the role of alpha2-antiplasmin (α2AP) in the progression of MAS.
- To explore α2AP's influence on macrophage activation and related inflammatory pathways.
Main Methods:
- Utilized a fulminant MAS mouse model induced by toll-like receptor-9 agonist (CpG) and D-(+)-galactosamine hydrochloride (DG).
- Assessed the effects of α2AP deficiency and blockade by neutralizing antibodies on MAS progression.
- Examined α2AP's impact on interferon-γ (IFN-γ)-induced macrophage migration and tissue factor production.
Main Results:
- α2AP deficiency attenuated macrophage accumulation, liver injury, and fibrin deposition in MAS model mice.
- α2AP enhanced IFN-γ-induced macrophage migration and tissue factor production.
- Fibrin induced macrophage activation and tumor necrosis factor-α production, which was modulated by α2AP.
Conclusions:
- α2AP plays a significant role in MAS progression by regulating IFN-γ-induced responses.
- α2AP is associated with increased macrophage activation and fibrin deposition in MAS.
- Targeting α2AP may offer a therapeutic strategy for managing MAS.
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