The mechanism of B cell activation in T cell-independent immune response

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K16700
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 49070:Immunology-related
• Research Institution: Tokyo University of Science
• Principal Investigator: Fukao Saori 東京理科大学, 研究推進機構生命医科学研究所, 研究員 (20778914)
• Project Period (FY): 2019-04-01 – 2021-03-31
• Keywords: B細胞 / T細胞非依存性免疫応答

Outline of Final Research Achievements

Antibody production by a T cell-independent type 2 (TI-2) immune response is necessary for the protection against infections such as Streptococcus pneumoniae and Salmonella. Here, we studied the molecular mechanism of antibody production in the TI-2 response by focusing on the signaling pathway specifically induced by the TI-2 antigen in B cells. We showed that the TI-2 antigen specifically induces the association of BCR with Prohibitin and the phosphorylation of PKCδ. Prohibitin was involved in B cell proliferation and PKCδ was required for a class switching to IgG. Therefore, the activation of signaling pathways mediated by these molecules would be important for protection against TI-2 antigens.

Free Research Field

B細胞免疫応答

Academic Significance and Societal Importance of the Research Achievements

肺炎球菌やサルモネラ菌に対する感染症は、乳幼児や高齢者において罹患率が高く、髄膜炎や敗血症などの併発によって重篤化しやすい。これらの菌は細胞壁外に多糖体からなる莢膜を持つために通常の免疫応答を誘導しにくく、TI-2免疫応答によって産生される抗体が感染防御に重要である。本研究によって明らかになった抗体産生の機構は、上述の菌に対するより効率的なワクチン開発の分子基盤になると期待される。