CD30 supports lung inflammation.

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 T(h)2 responses in the effector-memory phase and a regulator of IL-13 production in memory cells in the lung.