Format

Send to

Choose Destination
See comment in PubMed Commons below
J Allergy Clin Immunol. 2007 Dec;120(6):1324-31. Epub 2007 Sep 24.

Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma.

Author information

  • 1Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.

Abstract

BACKGROUND:

IL-25 (IL-17E), a member of the IL-17 family of immunoregulatory cytokines, has been implicated in the regulation of type 2 immunity. Its roles in antigen-driven airway inflammation and airway hyperresponsiveness (AHR) remain to be fully established.

OBJECTIVE:

We sought to determine whether a neutralizing antibody against IL-25 represents a novel therapeutic for airway inflammation and hyperresponsiveness.

METHODS:

We generated a neutralizing mAb against IL-25 and used this to inhibit IL-25 in a mouse model of allergic airway disease.

RESULTS:

Blocking IL-25 in an experimental model of allergic asthma prevented AHR, a critical feature of clinical asthma. Administration of anti-IL-25 mAb during the sensitization phase resulted in significantly reduced levels of IL-5 and IL-13 production, eosinophil infiltration, goblet cell hyperplasia, and serum IgE secretion, and prevented AHR. Even more striking was the ability of anti-IL-25 mAb, administered only during the challenge phase of the response, specifically to prevent AHR even during an ongoing type 2 inflammatory response in the lungs.

CONCLUSION:

IL-25 is critical for development of AHR.

CLINICAL IMPLICATIONS:

We define a novel pathway for the induction of AHR and suggest that IL-25 represents an important therapeutic target for the treatment of asthma. Significantly, our antibody also blocks the binding of human IL-25 to its receptor.

PMID:
17889290
DOI:
10.1016/j.jaci.2007.07.051
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center