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Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Regulatory T cells and systemic lupus erythematosus
P A Mudd1, B N Teague, A D Farris
1Arthritis and Immunology Research Program, Oklahoma Medical Research Foundation, 825 N.E. 13th Street, Oklahoma City, OK 73104, USA.
Scandinavian Journal of Immunology
|August 22, 2006
Summary
Regulatory T cells (Treg) are crucial for immune tolerance. Studies suggest Treg dysfunction, not just reduced numbers, may drive systemic lupus erythematosus (SLE) pathogenesis, particularly concerning Toll-like receptor activation.
Area of Science:
- Immunology
- Autoimmunity
- Cellular Biology
Background:
- CD4+CD25+ regulatory T cells (Treg) are vital for peripheral immune tolerance.
- Breakdown of Treg-mediated tolerance is implicated in organ-specific autoimmune diseases.
- The role of Treg in systemic lupus erythematosus (SLE) remains incompletely understood.
Purpose of the Study:
- To investigate the role and function of Treg in the context of SLE.
- To explore potential defects in Treg function in SLE patients and murine models.
- To examine the impact of Toll-like receptor (TLR) ligation on Treg function in SLE.
Main Methods:
- Utilizing advanced tools to differentiate Treg from activated T cells.
- Assessing Treg numbers and function in SLE patients and lupus-prone mice.
- Investigating the effects of TLR ligation (TLR-2, -4, -8, -9) on Treg-mediated suppression.
Main Results:
- Preliminary data suggest reduced Treg numbers in some SLE patients.
- Evidence indicates potential functional defects in SLE Treg.
- Thymic Treg proportions were found to be equivalent in lupus-prone and normal mice.
- Toll-like receptor ligation can abrogate Treg-mediated suppression.
Conclusions:
- Treg function, rather than mere numbers, is likely a critical factor in SLE pathogenesis.
- Dysfunctional Treg may contribute to the loss of self-tolerance in SLE.
- A model is proposed where TLR ligation contributes to Treg tolerance breakdown against nucleic acid-binding SLE autoantigens.
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