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The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin.
J Clin Invest. 1998 Dec 15; 102(12):2096-105.JCI

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.

Authors+Show Affiliations

Max-Planck Institut für physiologische und klinische Forschung, W.G. Kerckhoff-Institut, Bad Nauheim, Germany. bengelh@kerckhoff.mpg.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9854045

Citation

Engelhardt, B, et al. "The Development of Experimental Autoimmune Encephalomyelitis in the Mouse Requires Alpha4-integrin but Not Alpha4beta7-integrin." The Journal of Clinical Investigation, vol. 102, no. 12, 1998, pp. 2096-105.
Engelhardt B, Laschinger M, Schulz M, et al. The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin. J Clin Invest. 1998;102(12):2096-105.
Engelhardt, B., Laschinger, M., Schulz, M., Samulowitz, U., Vestweber, D., & Hoch, G. (1998). The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin. The Journal of Clinical Investigation, 102(12), 2096-105.
Engelhardt B, et al. The Development of Experimental Autoimmune Encephalomyelitis in the Mouse Requires Alpha4-integrin but Not Alpha4beta7-integrin. J Clin Invest. 1998 Dec 15;102(12):2096-105. PubMed PMID: 9854045.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin. AU - Engelhardt,B, AU - Laschinger,M, AU - Schulz,M, AU - Samulowitz,U, AU - Vestweber,D, AU - Hoch,G, PY - 1998/12/17/pubmed PY - 1998/12/17/medline PY - 1998/12/17/entrez SP - 2096 EP - 105 JF - The Journal of clinical investigation JO - J Clin Invest VL - 102 IS - 12 N2 - 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. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/9854045/The_development_of_experimental_autoimmune_encephalomyelitis_in_the_mouse_requires_alpha4_integrin_but_not_alpha4beta7_integrin_ L2 - https://doi.org/10.1172/JCI4271 DB - PRIME DP - Unbound Medicine ER -