Anti-HMGB1 monoclonal antibody therapy for a wide range of CNS and PNS diseases

Masahiro Nishibori, Shuji Mori, Hideo K. Takahashi

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

High mobility group box-1 (HMGB1), a representative damage associated-molecular pattern (DAMP), has been reported to be involved in many inflammatory diseases. Several drugs are thought to have potential to control the translocation and secretion of HMGB1, or to neutralize extracellular HMGB1 by binding to it. One of these drugs, anti-HMGB1 monoclonal antibody (mAb), is highly specific for HMGB1 and has been shown to be effective for the treatment of a wide range of CNS diseases when modeled in animals, including stroke, traumatic brain injury, Parkinson's disease, epilepsy and Alzheimer's disease. Thus, anti-HMGB1 mAb not only is useful for target validation but also has extensive potential for the treatment of the above-mentioned diseases. In this review, we summarize existing knowledge on the effects of anti-HMGB1 mAb on CNS and PNS diseases, the common features of translocation and secretion of HMGB1 and the functional roles of HMGB1 in these diseases. The existing literature suggests that anti-HMGB1 mAb therapy would be effective for a wide range of CNS and PNS diseases.

Original languageEnglish
JournalJournal of Pharmacological Sciences
DOIs
Publication statusPublished - Jan 1 2019

Fingerprint

Central Nervous System Diseases
Peripheral Nervous System Diseases
Monoclonal Antibodies
Therapeutics
Pharmaceutical Preparations
Parkinson Disease
Epilepsy
Alzheimer Disease
Stroke

Keywords

  • DAMP
  • Epilepsy
  • High mobility group box-1 (HMGB1)
  • Monoclonal antibody (mAb)
  • Neuroinflammation
  • Neuropathic pain
  • Stroke
  • TBI

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

Cite this

Anti-HMGB1 monoclonal antibody therapy for a wide range of CNS and PNS diseases. / Nishibori, Masahiro; Mori, Shuji; Takahashi, Hideo K.

In: Journal of Pharmacological Sciences, 01.01.2019.

Research output: Contribution to journalReview article

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