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Cited by 305

The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.

Anti-α4 integrin therapy for multiple sclerosis: Mechanisms and rationale

Rice, George P.A., Hartung, Hans-Peter, Calabresi, Peter A.·2005·Neurology

Abstract

The symptoms, severity, and course of multiple sclerosis (MS) vary among patients, leading to complex treatment issues. In recent years, research has focused on specific adhesion molecules that participate in the activation and function of lymphocytes, especially the migration of these cells to sites of inflammation. In particular, the integrin, very late activation antigen (VLA)-4, has been implicated in mediating adhesion and migration of immune cells through interaction with its ligand, vascular cell adhesion molecule (VCAM)-1. VLA-4 is comprised of alpha4/beta1 and is critical in mediating Th-1 cell migration in the animal model of MS, experimental autoimmune encephalomyelitis, and has been the target of several recent clinical trials in MS. The humanized monoclonal antibody to alpha4 integrin, natalizumab (Tysabri, Biogen Idec/Elan), was recently approved in the United States for the treatment of relapsing MS. The authors discuss the mechanisms by which alpha4 integrins alter lymphocyte function as a rationale for anti-alpha4 integrin use in MS.

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Metadata

Authors
Rice, G. P. A., Hartung, H.-P., & Calabresi, P. A.
Venue
Neurology
Published
2005-04-26
Volume
64
Issue
8
Pages
1336-1342
ISSN
  • 0028-3878 (ISSN-L)
  • 1526-632X
OpenAlex
W2059114092
Cited by
305
References
66
FWCI
14.19
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Anti-α4 integrin therapy for multiple sclerosis: Mechanisms and rationale. https://app.cochat.ai/papers/10.1212/01.wnl.0000158329.30470.d0
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Rice, G. P. A., Hartung, H.-P., & Calabresi, P. A. (2005). Anti-α4 integrin therapy for multiple sclerosis: Mechanisms and rationale. Neurology. https://doi.org/10.1212/01.wnl.0000158329.30470.d0

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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