Function of Special AT-Rich sequence binding protein 1 in B cells' tolerance

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K16115
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 54010:Hematology and medical oncology-related
• Research Institution: Osaka University
• Principal Investigator: Ozawa Takayuki 大阪大学, 医学部附属病院, 医員 (90815474)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: B 細胞

Outline of Final Research Achievements

In this study, we analyzed the role of SATB1 on mature B cells. SATB1 controls various genes' expression by remodeling chromatin architecture. By analyzing SATB1/tomato reporter mice, we found SATB1 high Naive B cells are more likely to activate against antigen stimulation than SATB1 low naive B ccells. We made B cell specific SATB1 knock out mice (cKO mice) and analyzed them. We found that naive B cells of cKO mice reduced expression of antigen presenting molecule such as MHC II and CD86 against B cell receptor stimulation. These results suggested that SATB1 helps naive B cells to be activated against antigen stimulation.

Free Research Field

B 細胞

Academic Significance and Societal Importance of the Research Achievements

この研究によって、SATB1がB細胞の免疫活性を調整する一つの要因であることがわかりました。B細胞の働きの異常は、自己免疫疾患や癌など、さまざまの病気の原因となることがわかっています。この研究でわかったSATB1とB細胞の関係は、こういった病気の新しい治療法を見つける糸口なる可能性があります。