CD30 supports lung inflammation

Sang Yun Nam, Young Hyun Kim, Jeong Su Do, Yun Hwa Choi, Hyo Jung Seo, Ho Keun Yi, Pyung Han Hwang, Chang Ho Song, Hern Ku Lee, Jeong Su Kim, Eckhard R. Podack

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


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-γ, 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.

Original languageEnglish (US)
Pages (from-to)177-184
Number of pages8
JournalInternational Immunology
Issue number2
StatePublished - Feb 2008


  • Asthma
  • Cytokines
  • T1/T2 cell
  • Transgenic/knockout mouse

ASJC Scopus subject areas

  • Immunology


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