Host-microbe interaction mediated by intestinal M cells

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293114
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Keio University (2014-2015); The University of Tokyo (2013)
• Principal Investigator: Hase Koji 慶應義塾大学, 薬学部, 教授 (20359714)
• Co-Investigator(Renkei-kenkyūsha): MIMURO Hitomi 東京大学, 医科学研究所, 准教授 (80396887) ; FURUSAWA Yukihiro 富山県立大学, 工学部, 講師 (80632306) ; KIMURA Shunsuke 北海道大学, 医学研究科, 助教 (40444525)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 粘膜免疫

Outline of Final Research Achievements

It remains unknown whether M-dependent antigen uptake also contributes to cellular immunity against mucosal pathogens. Here we investigated the contribution of M cells to Th17-dependent cellular immunity. Wild type (WT) and M-cell-null mice were orally infected with Citrobacter rodentium. After the infection, M-cell-null mice developed more severe infectious colitis compared to WT mice, as evidenced by exacerbation of body weight loss and fecal clinical scores. Importantly, colonic Th17 cells were decreased in M-cell-null mice compared to WT mice at the early phase of infection. In contrast, under the physiological conditions, there was no significant difference in the number of colonic Th17 cells between the two groups. Collectively, these results suggested that M-cell-dependent antigen uptake plays a key role in the protection against C. rodentium infection by facilitating antigen-specific Th17 induction.

Free Research Field

免疫学