The murine gammaherpesvirus-68 chemokine-binding protein M3 inhibits experimental autoimmune encephalomyelitis.

Abstract:

:Chemokines are critical mediators of immune cell entry into the central nervous system (CNS), as occurs in neuroinflammatory disease such as multiple sclerosis. Chemokines are also implicated in the immune response to viral infections. Many viruses encode proteins that mimic or block chemokine actions, in order to evade host immune responses. The murine gammaherpesvirus-68 encodes a chemokine-binding protein called M3, which has unique biochemical features that enable it to bind to and inhibit an unusually broad range of chemokines. We applied a replication-defective adenoviral vector encoding M3 (AdM3) directly to the CNS to evaluate the capacity of this protein to inhibit neuroinflammation using the experimental autoimmune encephalomyelitis (EAE) model. Treatment with the AdM3 vector significantly reduced the clinical severity of EAE, attenuated CNS histopathology, and reduced numbers of immune cells infiltrating the CNS. These results suggest that M3 may represent a novel therapeutic approach to neuroinflammatory disease.

journal_name

J Neuroimmunol

authors

Millward JM,Holst PJ,Høgh-Petersen M,Thomsen AR,Christensen JP,Owens T

doi

10.1016/j.jneuroim.2010.05.005

subject

Has Abstract

pub_date

2010-07-27 00:00:00

pages

45-50

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(10)00189-X

journal_volume

224

pub_type

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