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J Allergy Clin Immunol. 2006 Oct;118(4):942-8. Epub 2006 Sep 6.

Direct evidence for a critical role of CD30 in the development of allergic asthma.

Author information

1
Department of Pediatrics, Division of Pediatric Pulmonology and Neonatology, Medizinische Hochschule Hannover, Germany.

Abstract

BACKGROUND:

CD30 is a costimulatory molecule belonging to the TNF receptor superfamily that is expressed on activated T and B cells. Several studies have demonstrated a positive correlation between expression of CD30 or increased levels of soluble CD30 and the development and severity of allergic diseases. However, thus far, the evidence for a role of CD30 in allergic diseases, such as asthma, is only indirect.

OBJECTIVE:

The aim of the study was to directly investigate the role of CD30 in a murine asthma model.

METHODS:

CD30-deficient (B6.129P2-Tnfrsf8(tm1Mak)/J) and wild-type (WT) mice were immunized to ovalbumin (OVA) to induce an asthma-like phenotype and compared in our murine asthma model. Moreover, CD30/CD30 ligand signaling was blocked in OVA-immunized WT animals by using mAbs against CD30 receptor and its ligand, CD153.

RESULTS:

The absence of CD30 in OVA-immunized CD30-deficient mice resulted in significantly reduced airway inflammation, serum IgE levels, and TH2 cytokine levels. The same effect was observed when CD30/CD153 signaling was blocked in OVA-immunized WT animals with mAbs against CD30 or CD30 ligand.

CONCLUSION:

Our results directly demonstrate that CD30/CD153 interaction plays an important role in the induction of TH2 cell-mediated allergic asthma.

CLINICAL IMPLICATIONS:

These findings provide evidence for a role of the costimulatory molecule CD30 in allergic asthma.

PMID:
17030250
DOI:
10.1016/j.jaci.2006.07.014
[Indexed for MEDLINE]
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