| Project/Area Number |
15H06866
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Immunology
|
|---|
| Research Institution | Institute of Physical and Chemical Research |
|---|
Principal Investigator |
Satoh-Takayama Naoko 国立研究開発法人理化学研究所, 統合生命医科学研究センター, 研究員 (90732446)
|
|---|
| Research Collaborator |
Mimuro Hitomi 大阪大学, 微生物病研究所 (80396887)
|
|---|
| Project Period (FY) |
2015-08-28 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | ILCs / Microbiota / 粘膜免疫 / 自然リンパ球 / 免疫学 |
|---|
| Outline of Final Research Achievements |
Intestinal tract is recently well studied to lead immune-responses induced by commensal bacteria stimulation, whereas stomach have been missed the immunological function on account of believing for only having sterilization of foods. Here, we report that stomach is also playing as “functional responder” following dominance of type 2 innate lymphoid cells (ILC2s). Further, stomach-ILC2s are exposed to commensal bacteria “Bacterodales”, which is stationary forming population in mucin-layer of stomach. The clearance of pathogenic bacteria “Helicobacter pylori (H.pylori)” in stomach is also regulated by ILC2s-driven defense through IgA induction. Thus, ILC2s in stomach are key factor for regulating total microbiota symbiosis as first barrier.
|
