| Project/Area Number |
24790489
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Immunology
|
|---|
| Research Institution | Institute of Physical and Chemical Research |
|---|
Principal Investigator |
IMANISHI Takayuki 独立行政法人理化学研究所, 統合生命医科学研究センター, 研究員 (10513442)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | Th2 / TLR / Th1 / 共刺激 / サイトカイン |
|---|
| Research Abstract |
Nucleic acids (NAs) are recognized by Toll-like receptors, RIG-I-like receptors, and inflammasomes and then activate innate immune responses. NAs also induce T cell costimulation upon T cell receptor stimulation, but the mechanism and physiological function of this response remains unclear. Unlike in innate cells, T cell costimulation is induced even by self-DNA, which is released from dead cells and complexes with antimicrobial peptides or histones. Such NA complexes are internalized by T cells and induced costimulatory responses. The recognition of NAs and subsequent activation of T cells are independent of all known NA sensors in innate system. We found, crucially, that such NA-mediated costimulation induces Th2 differentiation from naive T cells by suppressing T-bet expression, followed by the induction of GATA-3 and Th2 cytokines. These findings provide unveiled function of NA sensing by T cells to trigger and amplify allergic inflammation.
|
