The collaborative research group administered "chemical mutagens" to mice to produce mutant mice.This mouse develops atopic dermatitis 8 to 10 weeks after birth even in a clean environment.When the gene mutation that causes the pathogenesis was investigated, a point mutation (one-base mutation) occurred in the gene sequence of the "JAK1" molecule, and the kinase activity, which is a phosphorylating enzyme of JAK1, increased (JAK1 molecule is found in various cells. Signal transduction factor of "cytokine" important for proliferation and differentiation).As a result, it was also found that the gene expression of the protease (peptide hydrolase) group expressed when the old keratin of the epidermal cells is peeled off before the onset is increased, and the skin barrier caused by the keratin is impaired.

　When JAK inhibitor was applied to the skin of these mice, the expression of protease was suppressed and the onset of atopic dermatitis was delayed.In addition, the onset could be prevented by applying Vaseline for an ointment substrate.At this time, the skin barrier function was maintained at the same level as normal, and the occurrence of inflammation in the dermis (fibrotic connective tissue under the epidermis) was suppressed.

　Using the mice produced this time, it is possible to clarify multiple factors involved in the onset of atopic dermatitis at the molecular and cellular levels, so it is expected to establish preventive and therapeutic methods for each target.

This study was published in the online version of the American scientific journal "Journal of Clinical Investigation" dated April 4.