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International Immunology Advance Access published online on December 18, 2007
International Immunology, doi:10.1093/intimm/dxm130
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

CD30 supports lung inflammation

Sang-Yun Nam1, Young-Hyun Kim1, Jeong-Su Do1, Yun-Hwa Choi1, Hyo-Jung Seo1, Ho-Keun Yi2, Pyung-Han Hwang2, Chang-Ho Song3, Hern-Ku Lee4, Jeong-Su Kim2 and Eckhard R. Podack5

1 Department of Biological Science, School of Science and Technology, Jeonju University, Jeonju 560-759, Korea
2 Department of Pediatrics
3 Department of Anatomy
4 Department of Immunology, Chonbuk National University School of Medicine, Jeonju 560-712, Korea
5 Department of Microbiology and Immunology, University of Miami, Miller School of Medicine, Miami, FL 33136, USA

Correspondence to: Correspondence to: E. R. Podack; E-mail: epodack{at}miami.edu

The physiological functions of CD30 have not been fully elucidated. Here we show that in CD30-deficient mice (CD30–/–), lung inflammation is significantly diminished in the ovalbumin (OVA) model of airway hyperreactivity. In CD30–/– mice, the recruitment of eosinophils into the airways after OVA–aerosol challenge of OVA-primed mice was significantly diminished when compared with wild-type (w.t.) mice. IL-13 levels were also significantly reduced in CD30–/– mice while levels of IFN-{gamma}, IL-4, IL-5 and IgE in bronchoalveolar lavage fluid, lung tissue and serum were comparable to w.t. mice. Peribronchial lymph node cells from CD30–/– mice, re-stimulated in vitro with OVA, secreted significantly lower levels of IL-13 than those from w.t. mice, but showed normal proliferative response and other cytokine production. Exogenous IL-13 reconstituted airway recruitment of leukocytes in OVA-challenged CD3O–/– mice. Adoptive transfer to naive w.t. mice of in vitro OVA-re-stimulated spleen cells from CD30–/– mice failed to induce eosinophilic pulmonary inflammation in contrast to transfer of primed cells from w.t. mice. These results indicate that CD30 is a regulator of Th2 responses in the effector–memory phase and a regulator of IL-13 production in memory cells in the lung.

Keywords: asthma, cytokines, Th1/Th2 cell, transgenic/knockout mouse

Transmitting editor: R. A. Flavell

Received 9 January 2007, accepted 6 November 2007.


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