| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥14,040,000 (Direct Cost: ¥10,800,000、Indirect Cost: ¥3,240,000)
|
|---|
| Outline of Final Research Achievements |
Many autoimmune diseases are characterized by loss of regulatory T cell (Treg) numbers or their function. Drug-induced hypersensitivity syndrome (DiHS), a distinct phenotype of severe drug eruptions, offers a unique opportunity to link impaired Treg function with subsequent development of autoimmune disease. Our longitudinal study demonstrates that selective depletion of CD14dimCD16+ patrolling monocytes (pMOs) sensing herpesviruses occurring at the acute stage is associated with Treg expansion. After clinical resolution, however, 'pathogenic' pMOs with potent ability to produce IL-6 are alternatively recruited and contribute to the eventual shift away from a Treg to a Th17 responses that is observed at the resolution stage. pMOs would be the major therapeutic target for inflammatory diseases characterized by the shift from a Treg to a Th17 development.
|
