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| INDUCTION OF RELAPSING PARALYSIS IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS BY BACTERIAL SUPERANTIGEN |
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| Author(s): BROCKE S, GAUR A, PIERCY C, GAUTAM A, GIJBELS K, FATHMAN CG, STEINMAN L |
| Source: NATURE Volume: 365 Issue: 6447 Pages: 642-644 Published: OCT 14 1993 |
| Times Cited: 189 References: 23 |
| Abstract: THE role of infection in the pathogenesis of clinical relapses that occur in most autoimmune diseases, including multiple sclerosis, remains to be established1,2. Experimental autoimmune encephalomyelitis (EAE) serves as a model for multiple sclerosis, with episodes of relapsing paralysis3-9. In certain strains of mice, T-lymphocytes expressing the Vbeta8 T-cell receptor (TCR)6-8 engage the amino-terminal epitope Ac1-11 of myelin basic protein, leading to EAE. The bacterial superantigen staphylococcal enterotoxin B (SEB) activates Vbeta8-expressing T cells. Here we show that after immunization with Ac1-11, or after transfer of encephalitogenic T-cell lines or clones reactive to Ac1-11, SEB induces exacerbation or relapses of paralytic disease in mice that are in clinical remission following an initial episode of paralysis, and triggers paralysis in mice with subclinical disease. Tumour necrosis factor has a critical role in the mechanism underlying SEB-induced exacerbation of disease, because anti-tumour necrosis factor antibody given in vivo delays the onset of paralysis triggered by SEB. On reactivation of autoaggressive cells through their T-cell receptor, superantigens may induce clinical relapses of autoimmune disease. |
| Document Type: Article |
| Language: English |
| Reprint Address: BROCKE, S (reprint author), STANFORD UNIV, MED CTR, SCH MED, DEPT NEUROL & NEUROL SCI, STANFORD, CA 94305 USA |
Addresses:
1. STANFORD UNIV, MED CTR, SCH MED, DEPT MED, STANFORD, CA 94305 USA |
| Publisher: MACMILLAN MAGAZINES LTD, PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW |
| Subject Category: Multidisciplinary Sciences |
| IDS Number: MB846 |
| ISSN: 0028-0836 |
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