Clinical management of patients with systemic lupus erythematosus (SLE) with different C1q-CIC and C3 concentrations
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Updated: Jun 12, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Jasenko Karamehic1, Djemo Subasic, Mersija Kasumovic
1Institute of Clinical immunology-Clinical Centre, University of Sarajevo, Bolnicka 25, 71000 Sarajevo, Bosnia and Herzegovina.
Insights
Systemic Lupus Erythematosus (SLE) is linked to complement system disorders, with C1q-containing immune complexes and C3 levels being crucial for diagnosis and treatment. Understanding these complement pathways aids in managing SLE progression and tissue damage.
Area of Science:
- Immunology
- Rheumatology
- Clinical Chemistry
Background:
- Systemic Lupus Erythematosus (SLE) is an autoimmune disease often associated with autoantibodies against self-antigens.
- A significant portion of SLE patients exhibit elevated levels of autoantibody-antigen complexes containing complement proteins, particularly C1q.
- Disruptions in the complement system, including hereditary deficiencies and mutations affecting classical, alternative, or lectin pathways, can contribute to SLE pathogenesis and tissue damage.
Purpose of the Study:
- To investigate the role of complement system activation and autoantibodies in Systemic Lupus Erythematosus (SLE).
- To assess the diagnostic and therapeutic significance of C1q-containing immune complexes (C1q-CIC) and C3 levels in SLE patient serum.
- To analyze serum samples from patients suspected of autoimmune diseases, with a focus on SLE.
Main Methods:
- Screening for antinuclear antibodies (ANA) using ANA-Indirect Immunofluorescence Assay (ANA-IFA).
- Characterization of ANA-positive samples through ANA-IFA titration, Enzyme-Linked Immunosorbent Assay (ELISA), and nephelometry.
- Analysis of numerous serum samples collected from various clinics within the Clinical Center of the University of Sarajevo.
Main Results:
- Elevated C1q-containing immune complexes and altered C3 levels are observed in SLE patients.
- Specific autoantibodies targeting complement components are present in the serum of SLE patients.
- The study highlights the diagnostic and therapeutic importance of monitoring C1q-CIC and C3 levels in SLE management.
Conclusions:
- Complement system activation and deficiencies play a significant role in the pathogenesis of Systemic Lupus Erythematosus.
- Determination of C1q-CIC and C3 levels in serum is vital for the clinical management of SLE patients.
- Further research into complement system involvement in SLE can lead to improved diagnostic and therapeutic strategies.
Abstract:
Over the third of SLE (Systemic Lupus Erythematosus) patients have a high level auto-antibodies-antigen complex that contains some complement proteins, especially C1q as the trigger protein in the classical complement activation pathway. So, the SLE, as an autoimmune disease, is certainly related to disorders caused by activation of complement system, that finally leads to tissue damage. It may also be caused by hereditary deficiency (complement genes mutations). In such case, some components of the complement system might be inactivated. There are mutations that cause disorders in each of three complement system activation pathways (classical, alternative and lectin).The serum samples of SLE patients show the presence of specific autoantibodies for some complement components. Today, for clinical management of SLE patients, determination of level of C1q-CIC and C3 complement component in serum specimens have great diagnostic and therapeutic importance. During the year 2000, we analyzed a numerous serum samples from patients suspected to autoimmune diseases (SLE especially). The samples were collected from several clinics in the Clinical Center of University of Sarajevo, mostly from Clinic of Infectious Diseases, Pediatrics, Internal Medicine and Gastroenterohepatology Clinic. Primary samples went through screening for the presence of ANA using ANA-IFA method and further characterization of ANA positive samples was carried out using IFA-ANA titration, ELISA and nephelometry.
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