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Procainamide-induced autoimmunity: Relationship to T-helper 2-type T-cell activation
1National Center for Safety Evaluation of Drugs, National Institutes for Food and Drug Control, The Beijing Key Lab for Pre-clinical safety evaluation of Drugs, Beijing, People's Republic of China.
Human & Experimental Toxicology
|July 26, 2017
Summary
Procainamide can trigger drug-induced autoimmunity (DIA), with genetic factors influencing susceptibility. Brown Norway rats showed higher sensitivity due to T-helper 2 responses and gene expression changes.
Area of Science:
- Immunology
- Toxicology
- Pharmacology
Background:
- Drug-induced autoimmunity (DIA) comprises adverse drug reactions with unclear mechanisms.
- Procainamide is known to cause autoimmune reactions, but the underlying processes are not fully understood.
Purpose of the Study:
- To investigate the cellular and genetic factors contributing to procainamide-induced autoimmune responses.
- To compare the susceptibility to procainamide-induced autoimmunity across different rat strains with varying genetic predispositions.
Main Methods:
- Comparison of three rat strains: T-helper (Th)2-predisposed (Brown Norway, BN), Th1-predisposed (Lewis, LEW), and non-predisposed (Sprague Dawley, SD).
- Assessment of autoimmune responses and immune mechanisms following procainamide administration.
Main Results:
- Significant strain-dependent differences in procainamide-induced autoimmunity were observed.
- Brown Norway (BN) rats were most sensitive, Sprague Dawley (SD) rats showed less sensitivity, and Lewis (LEW) rats were resistant.
- BN rats exhibited pronounced Th2-type responses and complex gene expression changes related to immune regulation, contributing to their susceptibility.
Conclusions:
- Genetic predisposition, particularly Th2-skewed immunity and specific gene expression profiles, influences susceptibility to procainamide-induced autoimmunity.
- Identified immune mechanisms in BN and SD rats may serve as potential biomarkers for predicting DIA across species.
- This research enhances understanding of the toxicological mechanisms underlying drug-induced autoimmune reactions.
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