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Research Article Free access | 10.1172/JCI4271

The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin.

B Engelhardt, M Laschinger, M Schulz, U Samulowitz, D Vestweber, and G Hoch

Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.de

Find articles by Engelhardt, B. in: JCI | PubMed | Google Scholar

Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.de

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Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.de

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Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.de

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Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.de

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Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.de

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Published December 15, 1998 - More info

Published in Volume 102, Issue 12 on December 15, 1998
J Clin Invest. 1998;102(12):2096–2105. https://doi.org/10.1172/JCI4271.
© 1998 The American Society for Clinical Investigation
Published December 15, 1998 - Version history
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Abstract

Because monoclonal antibodies (mAbs) directed against alpha4-integrin and VCAM-1 inhibit the development of experimental autoimmune encephalomyelitis (EAE) in vivo, it has been concluded that the successful therapeutic effect is due to interference with alpha4beta1/VCAM-1-mediated interaction of autoaggressive T cells with the blood-brain barrier. A possible role for alpha4beta7-integrin, or interference with other T cell mediated events during the pathogenesis of EAE, has not been considered. We have compared the effects of mAb therapy on the development of EAE in the SJL/N mouse, using a large panel of mAbs directed against alpha4, beta7, the alpha4beta7-heterodimer, and against VCAM-1. Although encephalitogenic T cells express both alpha4-integrins, mAbs directed against the alpha4beta7-heterodimer or against the beta7-subunit did not interfere with the development of EAE. In contrast, mAbs directed against alpha4 and VCAM-1 inhibited or diminished clinical or histopathological signs of EAE. Our data demonstrate for the first time that alpha4beta7 is not essential for the development of EAE. Furthermore, our in vitro studies suggest that the therapeutic effect of anti-alpha4-treatment of EAE might also be caused by inhibition of antigen-specific T cell proliferation.

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