English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Multiple sclerosis is a chronic, inflammatory, and demyelinating disease of the central nervous system characterized by the pathological infiltration of autoreactive leukocytes. Experimental autoimmune encephalomyelitis serves as a disease model for human multiple sclerosis in mouse and rat (Conlon et al., 1999). Experimental autoimmune encephalomyelitis is induced through sensitization with neuroantigens such as myelin oligodendrocyte glycoprotein that activates neuroantigen-reactive T cells in the peripheral lymphoid organs. These T cells subsequently migrate into the central nervous system and encounter endogenous neuroantigens, which reactivates them and leads to nerve demyelination. Thus, induction of encephalitogenic T cells and their migration into the central nervous system are critical for development of experimental autoimmune encephalomyelitis.

The Role of CCR7-Ligands in Developing Experimental Autoimmune Encephalomyelitis