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Updated: Jul 14, 2026
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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Altered signal transduction in SLE T cells
K Tenbrock1, Y-T Juang, V C Kyttaris
1Department of Pediatrics, Division of Rheumatology, University Hospital Münster, Münster, Germany. ktenbroc@uni-muenster.de
Rheumatology (Oxford, England)
|June 26, 2007
Summary
Systemic lupus erythematosus (SLE) alters T cells, rewiring their receptor complex and aggregating lipid rafts. This leads to abnormal signaling, affecting cytokine production and immune cell interactions, contributing to autoimmunity and infection susceptibility.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmune Diseases
Background:
- T cells play a crucial role in immune responses.
- Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune system dysfunction.
- Abnormalities in T cell signaling are implicated in the pathogenesis of SLE.
Purpose of the Study:
- To investigate the signaling abnormalities in T cells from patients with SLE.
- To understand how these abnormalities contribute to the disease's clinical manifestations.
Main Methods:
- Analysis of T cell receptor complex composition.
- Assessment of T cell surface membrane lipid raft aggregation.
- Evaluation of downstream signaling events and cytokine expression profiles.
Main Results:
- T cells in SLE patients exhibit a rewired T cell receptor complex, with FcRgamma replacing CD3 zeta.
- Aggregation of T cell surface membrane lipid rafts is observed in SLE T cells.
- These alterations lead to enhanced early signaling, modified downstream events, and altered cytokine profiles (IL-6, IL-10, IL-2, IFNy, CD40 ligand).
Conclusions:
- The observed T cell signaling abnormalities in SLE contribute to enhanced T cell help for B cells, promoting autoantibody production.
- Decreased interleukin-2 (IL-2) production in SLE T cells correlates with increased susceptibility to infections, reduced activation-induced cell death, and prolonged survival of autoreactive T cells.
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