2014 Fiscal Year Final Research Report
Host defense against bacterial infection in Notch/IL-7Ralpha axis and CD30L dependent manner.
| Project/Area Number |
25670213
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Bacteriology (including mycology)
|
|---|
| Research Institution | Kyushu University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Keywords | NOTCH / Bcl11b / IL-7R / IL-17A / IFN-γ / γδT細胞 / CD30L / CD30 |
|---|
| Outline of Final Research Achievements |
Early T cell precursors at the double-negative (DN) 2 or 3 stages in fetal thymus are committed to IL-17A or IFN-γ γδ T cells.We found that IL-17A γδ T cells developed directly from DN2b cells in Notch/Hes1, Notch/Bcl11b and Notch/IL-7Rα-dependent pathways, whereas two types of IFN-γ γδ T cells developed from DN2a or DN3 stage in fetal thymus, respectively. CD30 and CD30L were selectively expressed by IL-17A γδ T cells and the number was drastically reduced in CD30L or CD30 knock out mice. In vivo administration of soluble CD30 protein (CD30-Ig) impaired the early protection against Listeria monocytogenes or Mycobacterium bovis Bacillus Calmette-Guerin infection,while agonistic anti-CD30 monoclonal antibody enhanced the protection by activating the IL-17A γδ T cells. CD30L/CD30 signaling plays an important role in the activation of IL-17A γδ T cells at the early stage for protection against bacterial infection.
|
| Free Research Field |
細菌学
|
