Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2005 Jan 15;96(1):11-26.
doi: 10.1016/j.imlet.2004.07.017.

New insights into cell responses involved in experimental autoimmune encephalomyelitis and multiple sclerosis

Affiliations
Review

New insights into cell responses involved in experimental autoimmune encephalomyelitis and multiple sclerosis

Mohamed El Behi et al. Immunol Lett. .

Abstract

Animal models of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE) are inflammatory demyelinating diseases which comprise a heterogeneous group of disorders that affect the peripheral and central nervous systems. EAE presents close similarities with multiple sclerosis (MS), a chronic inflammatory disease affecting central nervous system (CNS) white matter. Many studies have shown EAE to be a particularly useful animal model for the understanding of both the mechanisms of immune-mediated CNS pathology and the progressive clinical course of multiple sclerosis. Previous data has underlined the importance of CD4+ T cell involvement in mediating the autoimmune processes associated with the destruction of myelin and the role of the T helper 1 (Th1) pattern of cytokine secretion. However, EAE studies have also demonstrated that other cells involved in innate and/or adaptive immune responses may also play a critical role in the early and progressive events of the immune reaction leading to inflammation and CNS damage. In this review, we present such new data and discuss their potent implication for future new therapeutical approaches.

PubMed Disclaimer

Similar articles

Cited by

Publication types

LinkOut - more resources