| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
Neuroimmunological disorders are involved in the pathogenesis of atopic dermatitis (AD), partly through enhanced sensory nerve-skin mast cell interaction. Cell adhesion molecule 1 (CADM1) is known to mediate nerve-mast cell interaction. In a hapten-induce AD mouse model, AD-like lesional mast cells expressed three-fold more CADM1 transcripts than non-lesional mast cells. In nerve-mast cell coculture, CADM1 overexpression in IC2 mast cells strengthened dorsal root ganglion neurite-IC2 cell adhesion and doubled the population of IC2 cells responding to nerve activation. Increased expression of CADM1 in mast cells appeared to be a cause of enhanced sensory nerve-mast cell interaction in a hapten-induced AD mouse model, and might be involved in stress-induced deterioration of human AD.
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