Elucidation of suppressive mechanisms of autoreactive B cells byCD4+CD25-LAG3+ regulatory T cells
| Project/Area Number |
23791106
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
膠原病・アレルギー・感染症内科学
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
|---|
| Keywords | 制御性T細胞 / 自己抗体 / 全身性エリテマトーデス / LAG3 / Egr2 |
|---|
| Research Abstract |
The aim of this project is to elucidate the role of Egr2-expressing CD4+CD25-LAG3+ regulatory T cells (LAG3 Treg) in regulation of autoantibody production. Adoptive transfer of LAG3 Treg from control MRL/+ mice to MRL/Faslpr lupus prone mice significantly suppressed the progression of nephritis and autoantibody production. Interestingly, LAG3 Treg co-expressed Egr2 and PD-L1, and LAG3 Treg from T-cell-specific Egr2 conditional knockout or PD1 knockout mice failed to suppress B cell antibody production. These findings elucidate that LAG3 Treg play a crucial role in preventing the excessive B cell responses via Fas/FasL and PD-1/PD-L1 interactions. By exploiting the capacity of LAG3+ Tregs, they may provide a new therapeutic method in autoantibody-mediated autoimmune diseases, including SLE.
|
Report
(3 results)
Research Products
(21 results)
-
-
-
-
-
-
-
[Journal Article]2012
Author(s)
Izawa S, Okamura T, Matsuzawa K, Ohkura T, Ohkura H, Ishiguro K, Noh JY, Kamijo K, Yoshida A, Shigemasa C, Kato M, Yamamoto K, Taniguchi SI
-
Journal Title
Clin Endocrinol (Oxf)
Volume: 79
Issue: 1
Pages: 35-42
DOI
Related Report
Peer Reviewed
-
-
-
-
-
-
-
-
-
-
-
-
-
-
