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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Methods and protocols to study T cell signaling abnormalities in human systemic lupus erythematosus
Vaishali R Moulton1, Mindy S Lo, George C Tsokos
1Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Methods in Molecular Biology (Clifton, N.J.)
|August 31, 2012
Summary
Systemic lupus erythematosus (SLE) involves abnormal T cell signaling, including altered T cell receptor (TCR/CD3) function and calcium responses. Understanding these defects, particularly TCR/CD3ζ chain dysfunction, is key to unraveling SLE pathophysiology.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmune Diseases
Background:
- Systemic lupus erythematosus (SLE) pathogenesis involves aberrant T lymphocyte function.
- T cell receptor (TCR/CD3)-mediated signaling is dysregulated in SLE T cells.
Purpose of the Study:
- To investigate the molecular mechanisms underlying T cell signaling abnormalities in SLE.
- To identify factors contributing to defective T cell function in SLE.
Main Methods:
- Analysis of T cell receptor (TCR/CD3)-mediated stimulation.
- Assessment of protein tyrosine phosphorylation and intracellular calcium flux.
- Evaluation of Interleukin-2 (IL-2) production.
Main Results:
- SLE T cells exhibit increased protein tyrosine phosphorylation with faster kinetics.
- Heightened calcium flux response and decreased IL-2 production observed in SLE T cells.
- Aberrant expression and function of the TCR/CD3ζ chain identified as central to T cell dysfunction.
Conclusions:
- T cell signaling defects, especially TCR/CD3ζ chain abnormalities, are critical in SLE pathogenesis.
- Simplified protocols are presented for studying these abnormalities and identifying contributing factors.
- Further research can elucidate genetic, molecular, and biochemical bases of aberrant immune cell function in SLE.
