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Choroid plexus-selective inactivation of adenosine A2A receptors protects against T cell infiltration and experimental autoimmune encephalomyelitis.


ABSTRACT:

Background

Multiple sclerosis (MS) is one of the most common autoimmune disorders characterized by the infiltration of immune cells into the brain and demyelination. The unwanted immunosuppressive side effect of therapeutically successful natalizumab led us to focus on the choroid plexus (CP), a key site for the first wave of immune cell infiltration in experimental autoimmune encephalomyelitis (EAE), for the control of immune cells trafficking. Adenosine A2A receptor (A2AR) is emerging as a potential pharmacological target to control EAE pathogenesis. However, the cellular basis for the A2AR-mediated protection remains undetermined.

Methods

In the EAE model, we assessed A2AR expression and leukocyte trafficking determinants in the

SUBMITTER: Zheng W 

PROVIDER: S-EPMC8855604 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature