title: Anti-IL-31 receptor antibody is shown to be a potential therapeutic option for treating itch and dermatitis in mice.
abstract: OBJECTIVE
  IL-31, which is described as a pruritogenic cytokine, is linked to the itching that is associated with allergic and non-allergic eczema, but the precise pruritogenic mechanism of IL-31 and its potential as a therapeutic target for atopic dermatitis (AD) have not been determined.
  
  
  METHODS
  We investigated the effects of existing drugs on the scratching behaviour induced by an i.v. injection of IL-31 to clarify whether IL-31 induced pruritus indirectly. In addition, we studied the effects of an anti-IL-31 receptor α subunit (anti-IL-31 receptor α) neutralizing antibody on chronic pruritus-inducing dermatitis in an AD-like model to determine whether IL-31 not only induces scratching behaviour, but is also the causative factor in an AD phenotype.
  
  
  RESULTS
  The scratching behaviour induced by an i.v. injection of IL-31 was inhibited by pretreatment with an anti-IL-31 receptor α-neutralizing antibody. In contrast, it was not inhibited significantly by a non-sedative antihistamine (terfenadine), immunosuppressants (dexamethasone and tacrolimus), or a μ-opioid receptor antagonist (naloxone). The anti-IL-31 receptor α-neutralizing antibody reduced the ear swelling and dermatitis score in a chronic pruritus-inducing AD-like model. Moreover, treatment with the anti-IL-31 receptor α-neutralizing antibody showed therapeutic effects on the dermatitis even if it was injected after the disease had developed.
  
  
  CONCLUSIONS
  Anti-IL-31 receptor α is a potential novel therapeutic approach for escaping from the itch-scratch cycle and also a treatment for dermatitis in AD.
authors.affiliation: Department of Pharmacotherapy, Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan; Research Division, Chugai Pharmaceutical Co., Ltd., Shizuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kasutani
authors.forename: E
authors.initials: E
authors.lastname: Fujii
authors.forename: S
authors.initials: S
authors.lastname: Ohyama
authors.forename: H
authors.initials: H
authors.lastname: Adachi
authors.forename: M
authors.initials: M
authors.lastname: Hasegawa
authors.forename: H
authors.initials: H
authors.lastname: Kitamura
authors.forename: N
authors.initials: N
authors.lastname: Yamashita
mesh_terms: D000818:Animals; D018926:Anti-Allergic Agents / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D003876:Dermatitis, Atopic / Q000188:drug therapy*; D005260:Female; D007378:Interleukins / Q000276:immunology; D008807:Mice, Inbred BALB C; D011537:Pruritus / Q000188:drug therapy*; D018123:Receptors, Interleukin / Q000276:immunology*; D011994:Recombinant Proteins / Q000276:immunology
chemical_list: D018926:Anti-Allergic Agents; D000911:Antibodies, Monoclonal; C488159:Il31ra protein, mouse; D007378:Interleukins; D018123:Receptors, Interleukin; D011994:Recombinant Proteins; C502588:interleukin-31, mouse