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The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
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CD47 Potentiates Inflammatory Response in Systemic Lupus Erythematosus
Jin Kyun Park1,2, Ye Ji Lee2, Ji Soo Park1
1Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology and College of Medicine, Medical Research Center, Seoul National University, Seoul 03080, Korea.
Cells
|June 2, 2021
Summary
CD47 protein is elevated in systemic lupus erythematosus (SLE) patients, contributing to inflammation. Targeting CD47 may offer a new therapeutic strategy for SLE.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by aberrant immune responses.
- The role of CD47, a transmembrane protein, in SLE pathogenesis remains incompletely understood.
- Investigating CD47's function is crucial for developing targeted therapies for SLE.
Purpose of the Study:
- To elucidate the role of CD47 in the inflammatory processes of SLE.
- To examine CD47 and SIRPα expression in SLE patients' peripheral blood mononuclear cells (PBMCs).
- To assess the impact of SLE serum and inflammatory cytokines on CD47 expression.
Main Methods:
- Monocytes and THP1 cells were stimulated with LPS, anti-CD47 antibody, or both to measure TNF-α production.
- CD47 expression on PBMCs was analyzed using flow cytometry.
- Sera from SLE patients and healthy controls (HCs) were screened for anti-CD47 autoantibodies.
Main Results:
- CD47 expression on monocytes was significantly higher in SLE patients compared to HCs (p < 0.001).
- Monocyte CD47 expression correlated positively with SLE disease activity (p = 0.019).
- Anti-CD47 antibodies were found at higher levels in SLE patients (p = 0.02).
Conclusions:
- CD47 is upregulated on monocytes in SLE and is associated with disease severity.
- CD47 signaling contributes to heightened inflammatory responses in SLE.
- Targeting CD47 presents a potential novel therapeutic avenue for SLE management.
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