The analysis of mechanism of interferon-induced IP-10 production in monocytes with proteasome deficiency.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K19700
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• Research Institution: Wakayama Medical University
• Principal Investigator: INABA YUTAKA 和歌山県立医科大学, 医学部, 助教 (00647571)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 自己炎症性疾患 / インターフェロン / JAK / STAT / 中條-西村症候群 / プロテアソーム

Outline of Final Research Achievements

Nakajo-Nishimura syndrome (NNS) patients derived peripheral blood monocytes produced larger amount of IP-10 than control cells after IFNγ stimulation. However, it remains unclear how proteasome disability enhances IFN signaling. By western blotting, IFNγ-induced phosphorylated JAK1 level in immortalized B cells was higher in NNS patients-derived cells than in control cells. In contrast, phosphorylated STAT1 level did not change after IFNγ stimulation in either of NNS patients-derived immortalized B cells and control cells. These results suggest that proteasome degradation of phosphorylated JAK1 is critical for IFN signaling in NNS.

Free Research Field

自己炎症性疾患