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Defective antigen-presenting cell function in patients with systemic lupus erythematosus
G C Tsokos1, B Kovacs, P P Sfikakis
1Walter Reed Army Medical Center, Washington, DC 20307-5100, USA.
Arthritis and Rheumatism
|April 1, 1996
Summary
Systemic lupus erythematosus (SLE) patients show defective antigen-presenting cell (APC) function, specifically reduced B7-1 expression, impacting immune responses. Enhancing costimulatory signals can improve these defective recall antigen responses in SLE.
Area of Science:
- Immunology
- Cell Biology
Background:
- Patients with systemic lupus erythematosus (SLE) often exhibit impaired in vitro immune responses to recall antigens.
- This defect is linked to antigen-presenting cell (APC) dysfunction, particularly in patients with normal responses to alloantigens.
Purpose of the Study:
- To further characterize the specific defect in APC function observed in patients with SLE.
- To investigate the role of costimulatory molecules in the impaired immune response.
Main Methods:
- Mononuclear cells (MNC) from SLE patients and healthy controls were stimulated with tetanus toxoid (TT), anti-CD3 (OKT3), or alloantigens.
- Proliferative and interleukin-2 responses were measured.
- Cell surface B7-1 expression was assessed via flow cytometry, and experiments involved co-culture with transfected P815 cells.
Main Results:
- SLE patients were categorized into responders (+/+) and non-responders (-/+) to TT.
- Non-responders showed reduced interferon-gamma-induced B7-1 expression on APCs.
- Defective responses to TT and OKT3 in SLE patients were partially restored by B7/BBl-transfected cells, indicating a costimulatory defect.
Conclusions:
- SLE-associated APC defects involve abnormalities in surface molecules like B7.
- IgG Fc receptors also play a role in modulating immune responses in SLE patients.
- These findings highlight potential therapeutic targets for improving immune function in SLE.