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Defective cellular immune responses in lupus nephritis
Journal of Clinical & Laboratory Immunology
|July 1, 1984
Summary
Patients with lupus nephritis (LN) show significant cellular immune deficiency, impacting T cells and skin reactivity. These defects are more severe in LN patients with nephrotic syndrome, suggesting immune dysregulation.
Area of Science:
- Immunology
- Nephrology
- Cellular Biology
Background:
- Systemic lupus erythematosus (SLE) is an autoimmune disease.
- Lupus nephritis (LN) is a severe manifestation of SLE affecting the kidneys.
- Cellular immune responses are crucial in managing autoimmune conditions.
Purpose of the Study:
- To compare cellular immune responses in patients with lupus nephritis (LN) versus chronic mesangial proliferative glomerulonephritis (CGN).
- To identify specific defects in cell-mediated immunity (CMI) in LN patients.
- To assess the impact of nephrotic syndrome (NS) on CMI in LN.
Main Methods:
- Studied cell-mediated immunity (CMI) in 12 LN patients and 11 CGN patients.
- Assessed delayed hypersensitivity skin reactivity to keyhole limpet haemocyanin (KLH).
- Measured T cell percentages, lymphocyte transformation to phytohaemagglutinin (PHA), and concanavalin A (Con A)-induced suppressor cell activity (SCA).
Main Results:
- LN patients exhibited significantly depressed CMI, including impaired skin reactivity, reduced T cells, and diminished PHA response.
- Suppressor cell activity (SCA) was significantly lower in LN patients compared to controls and CGN patients.
- LN patients with nephrotic syndrome (NS) showed more profound CMI defects than those without NS.
Conclusions:
- Patients with lupus nephritis have significant defects in cellular immune responses.
- These immune defects are more pronounced in LN patients with nephrotic syndrome.
- Findings suggest an immunoregulatory defect contributing to the pathogenesis of lupus nephritis.