A new murine model of SSc/SLE overlap syndrome

2017 Fiscal Year Final Research Report

• Project/Area Number: 16H06754
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Collagenous pathology/Allergology
• Research Institution: The University of Tokyo
• Principal Investigator: Akamata Kaname 東京大学, 医学部附属病院, 助教 (00779788)
• Project Period (FY): 2016-08-26 – 2018-03-31
• Keywords: 全身性強皮症 / 全身性エリテマトーデス / 動物モデル / Fli1 / KLF5

Outline of Final Research Achievements

Systemic sclerosis (SSc)/ systemic lupus erythematosus (SLE) overlapy syndrome is characterized by the low frequency of lupus nephritis and the high frequency of serositis, but the molecular mechanism underlying this observation has still remianed unknown. To investigate the molecular mechanism regulating the pathological interference between SSc and SLE, we decided to generate a new overlapy syndrome animal model, namely, Klf5+/-;Fli1+/- mice treated with imiquimod, in which double heterozygous loss of KLF5 and Fli1 induces SSc symptoms and imiquimod administration induces lupus symptoms. At the time of writing, we have demonstrated that Klf5+/-;Fli1+/- mice develop cardiac and intestinal symptoms similar to those of SSc without renal invovlement. Now, we are investigating whether imiquimod-induced lupus symptoms are modified in Klf5+/-;Fli1+/- mice. The histological analysis of the skin, lung, heart, kidney, esophagus, and intestine is now on going.

Free Research Field

膠原病、特に全身性強皮症