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Digestion of Whole Mouse Eyes for Multi-Parameter Flow Cytometric Analysis of Mononuclear Phagocytes
Published on: June 17, 2020
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Mononuclear phagocyte system dysfunction in murine SLE: abnormal clearance kinetics precede clinical disease
N L Meryhew1, C Shaver, R P Messner
1Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
The Journal of Laboratory and Clinical Medicine
|March 1, 1991
Summary
Systemic lupus erythematosus (SLE) mouse models show a consistent early defect in Fc-mediated immune clearance, preceding disease onset. Complement-mediated clearance varies, with impairment in some strains and accelerated clearance in others.
Area of Science:
- Immunology
- Autoimmunity
- Murine Models
Background:
- Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune system dysregulation.
- Previous studies suggest abnormal immune clearance in murine SLE models, but a consistent defect in mononuclear phagocyte function was not established.
- Understanding immune clearance mechanisms is crucial for elucidating SLE pathogenesis.
Purpose of the Study:
- To investigate the mechanisms of immune clearance in murine models of SLE.
- To evaluate complement- and Fc-mediated clearance functions using kinetic analysis.
- To determine if defects in immune clearance precede the clinical manifestation of disease.
Main Methods:
- Kinetic analysis of radiolabeled, immunoglobulin-sensitized red blood cell clearance in normal (BALB/c) and SLE-prone mice (BXSB, MRL-lpr/lpr, NZB, NZB/W).
- Evaluation of four clearance rate constants: k1 (complement-mediated sequestration), k2 (C3b deactivation/release), k4 (complement-dependent phagocytosis), and k3 (Fc-mediated sequestration/phagocytosis).
- Studies conducted on mice aged 4 weeks to 18 months, using complement-fixing rabbit anti-mouse red blood cell antibody.
Main Results:
- All four SLE-prone mouse strains exhibited significantly decreased Fc-mediated clearance (k3) compared to controls, evident by 6 months of age and preceding disease onset in NZB mice.
- Complement-mediated clearance abnormalities varied: impaired in MRL-lpr/lpr (decreased k1, k4) and NZB/W mice, but normal in BXSB mice.
- NZB and NZB/W mice showed accelerated clearance due to decreased C3b deactivation/release (k2), occurring as early as 2 months of age.
Conclusions:
- A uniform, early, and progressive defect in Fc-mediated immune clearance is a hallmark of the studied murine SLE models.
- Complement-mediated clearance defects are strain-specific, ranging from severe impairment to accelerated clearance.
- These immune clearance abnormalities precede serologic and clinical disease activity, highlighting their role in SLE pathogenesis.
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