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Updated: May 21, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Published on: November 1, 2015

A model for lupus brain disease.

Betty Diamond¹, Bruce T Volpe

¹Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, NY 11030, USA. bdiamond@nshs.edu

Immunological Reviews

|June 26, 2012

Summary

This summary is machine-generated.

Systemic lupus erythematosus (SLE) brain damage may not involve immune complexes. Instead, autoantibodies directly alter neuronal function, requiring a compromised blood-brain barrier for entry, offering new insights into lupus neuroinflammation.

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Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

Neuroimmunology
Autoimmune Diseases
Pathophysiology

Background:

Systemic lupus erythematosus (SLE) is an autoimmune disease where antibodies target self-antigens, causing immune complex formation and inflammation in peripheral organs.
This immune complex-mediated inflammation leads to tissue damage and destruction in various body parts.
However, the mechanisms of central nervous system (CNS) injury in SLE have remained unclear, differing from peripheral organ damage.

Purpose of the Study:

To present a novel paradigm for autoantibody-mediated brain damage in SLE.
To differentiate the mechanisms of CNS injury from peripheral organ damage in SLE.
To explore the role of autoantibodies and blood-brain barrier integrity in lupus-related brain disease.

Main Methods:

Review of existing literature on SLE pathophysiology and neuroinflammation.
Development of a theoretical model for antibody-mediated brain damage.
Analysis of the conditions under which antibodies access brain tissue.

Main Results:

Autoantibody-mediated brain disease in SLE may not rely on immune complex formation.
Antibodies appear to directly affect neuronal activation and survival pathways.
Antibody entry into the brain necessitates impaired blood-brain barrier integrity.

Conclusions:

The proposed paradigm suggests a distinct mechanism for CNS damage in SLE compared to peripheral tissues.
Impaired blood-brain barrier function is critical for autoantibodies to affect the brain.
This model has implications for understanding lupus brain disease and identifying potential therapeutic targets.