Related Experiment Video
Updated: Jun 19, 2026

12:04
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Infectious antibodies in systemic lupus erythematosus patients
Y Berkun1, G Zandman-Goddard, O Barzilai
1Safra Children Hospital, Sheba Medical Center, Tel-Hashomer, Israel. berkun@post.tau.ac.il
Lupus
|November 3, 2009
Summary
Infections may trigger systemic lupus erythematosus (SLE). This study found higher antibodies to cytomegalovirus IgM and Epstein-Barr virus early antigen IgG in SLE patients, suggesting infectious agents
Area of Science:
- Immunology
- Infectious Diseases
- Rheumatology
Background:
- Infections are suspected environmental triggers for systemic lupus erythematosus (SLE) in genetically susceptible individuals.
- Recent advancements allow simultaneous testing of multiple antibodies, aiding in understanding SLE induction mechanisms.
Purpose of the Study:
- To compare the prevalence and titers of antibodies to various infectious agents between SLE patients and healthy controls.
- To investigate the role of specific infectious agents in the pathogenesis of SLE.
Main Methods:
- Sera from 120 SLE patients and 140 controls were analyzed using the BioPlex 2200 Multiplexed Immunoassay.
- Antibody levels against eight infectious agents (Epstein-Barr virus, cytomegalovirus, Toxoplasma gondii, rubella, Treponema pallidum, herpes simplex virus, hepatitis C virus, hepatitis B virus) were quantified.
Main Results:
- Cytomegalovirus IgM and Epstein-Barr virus early antigen IgG were significantly more prevalent in SLE patients.
- Hepatitis B core and rubella IgG antibodies were less prevalent in SLE patients.
- Elevated titers of cytomegalovirus IgM, Toxoplasma gondii IgG, Epstein-Barr virus early antigen IgG, and viral capsid antigen IgG were observed in SLE patients.
Conclusions:
- Previous exposure to certain infectious agents may be implicated in the induction or prevention of SLE.
- Specific viral and parasitic antibody profiles differentiate SLE patients from controls, highlighting potential roles in disease development.
