Regulatory mechanism for the differentiation and function of innate-like B cells

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460570
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Niigata University
• Principal Investigator: Touma Maki 新潟大学, 自然科学系, 助教 (40542246)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: B細胞 / 自然免疫

Outline of Final Research Achievements

Peritoneal B-1 cells and splenic marginal zone B cells that show rapid response to innate immune signals are called innate-like B cells. We investigated regulatory mechanisms for the differentiation and function of innate-like B cells focused on the role of IκBNS that is an atypical IκB molecule necessary for differentiation of these B cells. As a result, it was suggested that IκBNS is involved in the control of signal intensity via B cell receptor, which is considered important for differentiation of B-1 cells and marginal zone B cells. Innate-like B cells are also known as IL-10-producing B cell subsets. In this study, it was revealed that IκBNS is selectively required for IL-10 production in B cells responding to Toll-like receptor signals.

Free Research Field

免疫学