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Related Experiment Video

Updated: Jun 13, 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

Complement deficiency and systemic lupus erythematosus: consensus and dilemma.

Maryam Kallel-Sellami¹, Lilia Laadhar, Yousr Zerzeri

¹Department of Immunology, La Rabta Hospital, El Jaabari, 1007 Tunis, Tunisia. maryam_kallel@yahoo.com

Expert Review of Clinical Immunology

|May 19, 2010

Summary

Complement deficiencies in the classical pathway are linked to systemic lupus erythematosus (SLE). Understanding this connection offers new therapeutic targets for autoimmune disease modulation.

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

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

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Published on: June 8, 2022

Area of Science:

Immunology
Autoimmunity
Complement System

Background:

The role of the complement system in autoimmune diseases is debated.
Complement abnormalities are strongly linked to systemic lupus erythematosus (SLE).
Deficiencies in classical complement pathway components (C1q, C1r, C1s, C4A, C4B, C2) increase SLE susceptibility.

Purpose of the Study:

To review the relationship between complement deficiency and SLE.
To focus on deficiencies within the classical complement pathway.
To discuss the paradoxical role of the complement system in lupus.

Main Methods:

Literature review of complement deficiency and SLE.
Analysis of data on classical complement pathway components.
Discussion of the dual role of the complement system.

Main Results:

Classical complement pathway deficiencies are causally associated with SLE development.
These deficiencies often lead to early-onset SLE, bacterial infections, and negative anti-dsDNA antibodies.
The severity and association strength vary among different protein deficiencies.

Conclusions:

Complement deficiency presents a paradox in lupus pathogenesis, acting as both protective and detrimental.
The complement system aids in clearing immune complexes and apoptotic cells, linking its deficiency to lupus.
Understanding complement's role provides potential therapeutic targets for immune response modulation in SLE.