In this study, we investigated the potential role of CD26 in ovalbumin (OVA)-induced airway inflammation using CD26 gene knockout mice. Compared with WT counterparts, CD26(-/-) mice showed an obviously enhanced tissue response and denser pulmonary infiltrates containing eosinophils around vessels and in the parenchyma after OVA sensitization and challenge. Serum IgG, including subclasses IgG1 and IgG2a, was greatly reduced in CD26(-/-) mice, but serum IgE remained unchanged. CD26(-/-) mice had increased mRNA expression of the Th2 cytokines IL-4, IL-5, and IL-13 in the lungs compared with WT mice, whereas the levels of the pro-Th1 cytokine IL-12p40 were similar in both strains. Consequently, enhanced protein secretion of IL-4, IL-5, and IL-13 was detected in bronchoalveolar lavage (BAL) fluid from CD26(-/-) mice. In agreement with overexpressed Th2 cytokines, both mRNA transcript and protein levels of chemokines eotaxin and RANTES, as well as their receptors CC chemokine receptor 3 (CCR3) and CCR5, were elevated in CD26(-/-) mice. These results suggest a protective role for CD26 in restricting OVA-induced airway inflammation.
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