the elucidation of complication mechanism in patients with recessive dystrophic epidermolysis bullosa (RDEB)

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19724
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• Research Institution: Okayama University
• Principal Investigator: Tenta Ai (梶田藍) 岡山大学, 医学部, 客員研究員 (80770320)
• Research Collaborator: MORIZANE Shin 岡山大学病院, 皮膚科, 講師 (80423333)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 表皮角化細胞 / 真皮線維芽細胞 / Toll様受容体 / IL-6 / 血清アミロイドA

Outline of Final Research Achievements

We found that patients with recessive dystrophic epidermolysis bullosa (RDEB) have persistently higher levels of serum amyloid A (SAA) and IL-6 in the serum. Furthermore, we demonstrated that Toll-like receptor (TLR) ligands induce SAA expression via NF-kB in epidermal keratinocytes and dermal fibroblasts, and that SAA induces its own expression via TLR1/2 in these cells. Our results provide new evidence that the skin’s innate immune response contributes to the production of SAA, which might lead to an increased risk of systemic complications such as secondary amyloidosis of recessive dystrophic epidermolysis bullosa.

Free Research Field

表皮角化細胞、真皮線維芽細胞の免疫学的応答