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Prednisone and plasma exchange improve suppressor cell function in chronic inflammatory demyelinating polyneuropathy
G De Luca1, A Lugaresi, C Iarlori
1Center for Neuromuscular Diseases, Department of Oncology and Neuroscience, University of Chieti, Policlinico Clinicizzato Colle Dell'Ara, Italy.
Journal of Neuroimmunology
|May 6, 1999
Summary
Defective suppressor cell function in chronic inflammatory demyelinating polyneuropathy (CIDP) improves with prednisone and plasma exchange. This treatment normalizes suppressor cell function, correlating with clinical recovery in CIDP patients.
Area of Science:
- Immunology
- Neurology
- Clinical Medicine
Background:
- Chronic inflammatory demyelinating polyneuropathy (CIDP) is associated with defective Concanavalin A (ConA)-induced suppressor cell function.
- The role of this defect in CIDP disease activity and its importance in recovery remain to be fully elucidated.
Purpose of the Study:
- To investigate the modifications of ConA-induced suppressor cell function following treatment in patients with CIDP.
- To assess the correlation between changes in suppressor cell function and clinical improvement.
Main Methods:
- Studied 20 patients diagnosed with CIDP.
- Monitored ConA-induced suppressor cell function before and after treatment with prednisone and plasma exchange.
- Assessed clinical improvement in parallel with immunological marker changes.
Main Results:
- Treatment with prednisone and plasma exchange led to a significant increase in ConA-induced suppressor cell function, moving towards normal levels.
- The improvement in suppressor cell function was concurrent with observed clinical improvement in the patients.
- These findings suggest a potential mechanism involving the induction of suppression through cytokine network modulation.
Conclusions:
- Prednisone and plasma exchange may restore ConA-induced suppressor cell function in CIDP patients.
- The restoration of suppressor cell function appears to be linked to clinical recovery in CIDP.
- Modulation of the cytokine network or other humoral mediators could underlie the therapeutic efficacy of these treatments in CIDP.