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PLoS One. 2014 Feb 28;9(2):e90117. doi: 10.1371/journal.pone.0090117. eCollection 2014.

Antibody-mediated inhibition of TNFR1 attenuates disease in a mouse model of multiple sclerosis.

Author information

  • 1Department of Neuro-oncology, University Clinic Heidelberg, Heidelberg, Germany.
  • 2Institute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
  • 3Department of Neurology, Medical University of Graz, Graz, Austria.
  • 4Department of Neurology, University of the Saarland, Homburg/Saar, Germany.

Abstract

Tumour necrosis factor (TNF) is a proinflammatory cytokine that is known to regulate inflammation in a number of autoimmune diseases, including multiple sclerosis (MS). Although targeting of TNF in models of MS has been successful, the pathological role of TNF in MS remains unclear due to clinical trials where the non-selective inhibition of TNF resulted in exacerbated disease. Subsequent experiments have indicated that this may have resulted from the divergent effects of the two TNF receptors, TNFR1 and TNFR2. Here we show that the selective targeting of TNFR1 with an antagonistic antibody ameliorates symptoms of the most common animal model of MS, experimental autoimmune encephalomyelitis (EAE), when given following both a prophylactic and therapeutic treatment regime. Our results demonstrate that antagonistic TNFR1-specific antibodies may represent a therapeutic approach for the treatment of MS in the future.

PMID:
24587232
[PubMed - in process]
PMCID:
PMC3938650
Free PMC Article

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