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

Jason M Millward; Peter J Holst; Mette Høgh-Petersen; Allan R Thomsen; Jan P Christensen; Trevor Owens

doi:10.1016/j.jneuroim.2010.05.005

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

Jason M Millward, Peter J Holst, Mette Høgh-Petersen, Allan R Thomsen, Jan P Christensen, Trevor Owens

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

6 Citationer (Scopus)

Abstract

Udgivelsesdato: 2010-Jul

Originalsprog	Engelsk
Tidsskrift	Journal of Neuroimmunology
Vol/bind	224
Udgave nummer	1-2
Sider (fra-til)	45-50
Antal sider	5
ISSN	0165-5728
DOI	https://doi.org/10.1016/j.jneuroim.2010.05.005
Status	Udgivet - 2010

Bibliografisk note

Adgang til dokumentet

10.1016/j.jneuroim.2010.05.005

Citationsformater

The murine gammaherpesvirus-68 chemokine-binding protein M3 inhibits experimental autoimmune encephalomyelitis. / Millward, Jason M; Holst, Peter J; Høgh-Petersen, Mette; Thomsen, Allan R ; Christensen, Jan P; Owens, Trevor.

I: Journal of Neuroimmunology, Bind 224, Nr. 1-2, 2010, s. 45-50.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

@article{fd523ef0d77711df825b000ea68e967b,

title = "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.",

author = "Millward, {Jason M} and Holst, {Peter J} and Mette H{\o}gh-Petersen and Thomsen, {Allan R} and Christensen, {Jan P} and Trevor Owens",

note = "Keywords: Adenoviridae; Animals; Cell Line; Cell Migration Inhibition; Chemokines; Encephalomyelitis, Autoimmune, Experimental; Female; Gene Therapy; Gene Transfer Techniques; Genetic Vectors; Humans; Mice; Mice, Inbred C57BL; Protein Binding; Rhadinovirus; Severity of Illness Index; Treatment Outcome; Viral Proteins",

year = "2010",

doi = "10.1016/j.jneuroim.2010.05.005",

language = "English",

volume = "224",

pages = "45--50",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier",

number = "1-2",

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TY - JOUR

T1 - The murine gammaherpesvirus-68 chemokine-binding protein M3 inhibits experimental autoimmune encephalomyelitis

AU - Millward, Jason M

AU - Holst, Peter J

AU - Høgh-Petersen, Mette

AU - Thomsen, Allan R

AU - Christensen, Jan P

AU - Owens, Trevor

N1 - Keywords: Adenoviridae; Animals; Cell Line; Cell Migration Inhibition; Chemokines; Encephalomyelitis, Autoimmune, Experimental; Female; Gene Therapy; Gene Transfer Techniques; Genetic Vectors; Humans; Mice; Mice, Inbred C57BL; Protein Binding; Rhadinovirus; Severity of Illness Index; Treatment Outcome; Viral Proteins

PY - 2010

Y1 - 2010

N2 - 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.

AB - 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.

U2 - 10.1016/j.jneuroim.2010.05.005

DO - 10.1016/j.jneuroim.2010.05.005

M3 - Journal article

C2 - 20537410

VL - 224

SP - 45

EP - 50

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -