| Project/Area Number |
15K09519
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Collagenous pathology/Allergology
|
|---|
| Research Institution | University of Tsukuba |
|---|
Principal Investigator |
Tsuboi Hiroto 筑波大学, 医学医療系, 講師 (80580505)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | IgG4関連疾患 / シェーグレン症候群 / ケモカイン / CCL18 / CCR8 / 口唇唾液腺 / 涙腺 |
|---|
| Outline of Final Research Achievements |
We clarified that CCL18 expressing macrophages, dendritic cells, and plasmacytes were significantly increased in labial salivary glands (LSGs) of IgG4-related disease (IgG4-RD) compared with Sjögren’s syndrome (SS) and healthy controls (HC). In LSGs of IgG4-RD and SS, T, B cells and plasmacytes expressed CCR8 which is a receptor for CCL18, whereas not in LSGs of HC. Peripheral blood mononuclear cells (PBMCs) and peripheral B cells stimulated with CD40L, IL-4, IL-10, and IL-21 significantly highly produced IgG4 compared with those stimulated with CD40L and IL-4. Moreover addition of CCL18 enhanced IgG4 production from PBMCs and peripheral B cells stimulated with CD40L, IL-4, IL-10, and IL-21. These findings suggested that the CCL18-CCR8 axis might be a novel therapeutic target for IgG4-RD.
|
