Resistance and susceptibility to experimental autoimmune neuritis in Sprague-Dawley and Lewis rats correlate with different levels of autoreactive T and B cell responses to myelin antigens
✍ Scribed by Jie Zhu; Li-Ping Zou; Moiz Bakhiet; Eilhard Mix
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 277 KB
- Volume
- 54
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Experimental autoimmune neuritis (EAN) is a CD4 ؉ T cell-mediated, inflammatory demyelinating disease of the peripheral nervous system (PNS) that serves as a model for Guillain-Barre ´syndrome (GBS) in humans. Various mouse and rat strains show different susceptibilities to EAN that can be induced by immunization with bovine PNS myelin (BPM) ؉ Freund's complete adjuvant (FCA). We examined PNS-induced T and B cell responses and cytokine protein production as well as mRNA expression to study the mechanisms behind susceptibility to EAN in Lewis rats and resistance in Sprague-Dawley (SD) rats. Lewis rats with EAN have elevated PNS myelin-reactive interferon-␥ (IFN-␥) production, TNF-␣ mRNA expression, and increased B cell responses to PNS myelin antigens, but low PNS myelin-reactive transforming growth factor- (TGF-) and interleukin (IL)-10 mRNA expression in lymph node mononuclear cells (MNC). In contrast, resistance to EAN in SD rats is associated with reduced BPM and P2 peptide-reactive IFN-␥ production, TNF-␣ mRNA expression, and suppressed B cell responses to PNS myelin antigens as well as up-regulation of TGF- and IL-10 mRNA expression. Resistance to EAN is also associated with low-grade inflammation or absence of histological evidence of EAN. These results suggest that differential autoreactive T and B cells responses to PNS myelin antigens are strain specific, and the susceptibility to EAN is related to quantitative rather than qualitative differences in distribution between proinflammatory and anti-inflammatory cytokines. J.