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TRIM Expression and Its Association With Disease Activity in Systemic Lupus Erythematosus
Ling-Ying Lu1, Ling-Jung Yen1, Hui-Ling Hsia1
1Division of Allergy, Immunology, and Rheumatology, Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
The Kaohsiung Journal of Medical Sciences
|June 23, 2026
Summary
Specific tripartite motif-containing protein (TRIM) gene expression is inversely linked to systemic lupus erythematosus (SLE) disease activity and symptoms, suggesting TRIM proteins may serve as potential biomarkers for SLE progression and treatment monitoring.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmune Diseases
Background:
- Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by diverse clinical manifestations.
- Autoantibodies are central to SLE pathogenesis, but their levels do not consistently correlate with disease severity.
- The tripartite motif-containing protein (TRIM) family plays a role in immune regulation, with some TRIM proteins implicated in SLE, though their broader roles remain under investigation.
Purpose of the Study:
- To investigate the expression patterns of TRIM family proteins in patients with SLE.
- To evaluate the potential of TRIM proteins as biomarkers for SLE disease activity, clinical manifestations, and renal involvement.
- To explore the association between TRIM expression and hydroxychloroquine treatment in SLE patients.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) were collected from patients with SLE (n=33) and healthy controls (n=20).
- Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression levels of various TRIM genes.
- Statistical analyses were performed to correlate TRIM expression with SLE disease activity, clinical features, laboratory parameters, and treatment status.
Main Results:
- Elevated expression of TRIM5, TRIM11, TRIM21, and TRIM72 was observed in patients with inactive SLE, nonnephritic disease, or low disease activity compared to those with active or relapsed disease and healthy controls.
- TRIM gene expression levels showed a significant inverse correlation with clinical symptoms of SLE but not with laboratory parameters.
- Hydroxychloroquine users demonstrated higher TRIM21 expression levels compared to nonusers.
Conclusions:
- Specific TRIM proteins are inversely associated with SLE disease activity and clinical phenotypes, highlighting their potential utility as biomarkers.
- TRIM proteins may offer novel targets for assessing SLE progression and developing therapeutic strategies.
- Hydroxychloroquine treatment might influence TRIM21 expression, warranting further mechanistic studies.
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