Millions of people in the world are suffering from atopic dermatitis (AD), which is a chronic inflammatory skin disease triggered by Th2 immune responses. The NC/Nga mouse is the most extensively studied animal model of AD. Like human AD, NC/Nga mice demonstrate increased levels of IgE, a hallmark of Th2 immune responses. Adaptive immunity cannot be generated without help of innate immunity. Especially natural killer T (NKT) cells and marginal zone B (MZB) cells have been known to play important roles in linking innate immunity to adaptive immunity.

Through flow cytometric analysis and ELISA assay, we investigated whether these lymphocytes might be altered in number in NC/Nga mice.

Our data demonstrated that the number of NKT cells was reduced in NC/Nga mice and IFNγ production by NKT cells upon α-GalCer stimulation decreased to the levels of CD1d KO mice lacking in NKT cells. However, reduction of NKT cells in NC/Nga mice was not due to CD1d expression, which was normal in the thymus. Interestingly, there was a significant increase of CD1d^highB220⁺ cells in the spleen of NC/Nga mice. Further, we confirmed that CD1d^highB220⁺ cells are B cells, not dendritic cells. These CD1d^highB220⁺ B cells show IgM^highCD21^highCD23^low, a characteristic phenotype of MZB cells.

We provide the evidence that there are decreased activities of NKT cells and increased number of MZB cells in the NC/Nga mice. Our findings may thus explain why NC/Nga mice are susceptible to AD.