| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Outline of Final Research Achievements |
Combined hematopoietic loss of SOCS1 and SOCS3 causes rapid inflammatory disease in the syngeneic bone marrow transplantation. Loss of SOCS1 increases the number of CD8+CD44high cells. The expression of homing markers on these T cells may facilitate migration to organs and tissues, and the propensity for production of pro-inflammatory cytokines and chemokines, such as RANTES, MIP1a, GM-CSF and IL-3 for recruiting myeloid cells, as well as development of high circulating G-CSF concentrations, can account for the pathological infiltration of neutrophils, monocytes, eosinophils and lymphocytes at the numerous sites of inflammation in SOCS1KO mice. Our data extend the model to suggest that the absence of SOCS3 in the already pro-inflammatory environment established by SOCS1 deficiency, results in hyper-responsiveness of immune cells to cytokines such as G-CSF and IL-6, and dramatically accelerates myeloid proliferation and inflammatory infiltration of target tissues.
|
