Mice lacking the transcription factor RelB develop T cell-dependent skin lesions similar to human atopic dermatitis

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Abstract
Mice with a targeted disruption of the Rel / NF‐κB family member RelB develop a complex inflammatory phenotype and hematopoietic abnormalities. RelB‐deficient (relB– / –) mice were clinically normal until 4 – 10 weeks after birth when thickening of the skin and hair loss developed. Histological and immunohistochemical evaluation of relB– / – skin lesions revealed hyperkeratosis and marked epidermal hyperplasia. Many CD4+ T cells and eosinophils mixed with lesser numbers of CD8+ T cells and neutrophils were present in the dermis. There was a moderate increase of MHC class II‐positive dermal dendritic cells and dermal mast cells. Increased expression of Th2 cytokines correlated with increased mRNA levels of eotaxin and CCR3 in relB– / – skin. The dermatitis did not develop in the offspring of relB– / – mice crossed with transgenic mice that lack peripheral T cells, demonstrating that the skin lesions were T cell dependent. The dermatitis observed in RelB‐deficient mice had many similarities with atopic dermatitis in human patients including infiltrating CD4+ T cells and eosinophils in the skin, increased number of eosinophils in the blood and increased serum IgE. Thus, the relB– / – mouse should be a useful model to study the pathogenesis of this common allergic human disease.

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