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Updated: Jul 1, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
Tumor necrosis factor‑α in systemic lupus erythematosus: Structure, function and therapeutic implications (Review)
Farid Ghorbaninezhad1, Patrizia Leone2, Hajar Alemohammad3
1Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, East Azerbaijan 5165665811, Iran.
Tumor necrosis factor-alpha (TNF-α) plays a dual role in systemic lupus erythematosus (SLE) pathogenesis, acting as both an immune regulator and a pro-inflammatory mediator. Anti-TNF-α therapies show potential efficacy and safety in SLE treatment.
Area of Science:
- Immunology
- Rheumatology
- Pathophysiology
Background:
- Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine implicated in autoimmune diseases.
- Its precise role in complex conditions like systemic lupus erythematosus (SLE) remains incompletely understood.
- TNF-α exerts diverse biological effects via TNF receptor 1 (TNFR1) and TNF receptor 2 (TNFR2).
Purpose of the Study:
- To review the dual role of TNF-α in the pathogenesis of SLE.
- To explore the differential effects of TNF-α on SLE.
- To discuss the efficacy and safety of anti-TNF-α therapies in SLE.
Main Methods:
- Literature review of TNF-α's function in SLE.
- Analysis of TNF-α's impact on immune cells (B, T, dendritic cells).
- Evaluation of preclinical and clinical trial data for anti-TNF-α therapies in SLE.
Main Results:
- TNF-α acts as both an immune regulator and a pro-inflammatory mediator in SLE.
- Soluble and transmembrane TNF-α variants have distinct effects depending on the context.
- Anti-TNF-α therapies have demonstrated efficacy and safety in SLE management.
Conclusions:
- TNF-α has a complex, context-dependent role in SLE pathogenesis.
- Targeting TNF-α represents a viable therapeutic strategy for SLE.
- Further research is warranted to fully elucidate TNF-α's mechanisms in SLE.
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