科研之友
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摘要
Background and PurposeIL-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. Experimental ApproachWe 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 subunit (anti-IL-31 receptor ) 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. Key ResultsThe scratching behaviour induced by an i.v. injection of IL-31 was inhibited by pretreatment with an anti-IL-31 receptor -neutralizing antibody. In contrast, it was not inhibited significantly by a non-sedative antihistamine (terfenadine), immunosuppressants (dexamethasone and tacrolimus), or a -opioid receptor antagonist (naloxone). The anti-IL-31 receptor -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 -neutralizing antibody showed therapeutic effects on the dermatitis even if it was injected after the disease had developed. Conclusions and ImplicationsAnti-IL-31 receptor is a potential novel therapeutic approach for escaping from the itch-scratch cycle and also a treatment for dermatitis in AD.
- 出版日期2014-11
