The therapeutic effect of anti-Kim-1 antibody in lupus nephritis
Project/Area Number |
24791012
|
Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
膠原病・アレルギー・感染症内科学
|
Research Institution | Kinki University |
Principal Investigator |
NOZAKI Yuji 近畿大学, 医学部, 講師 (90411595)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
|
Keywords | lupus nephritis, RMT1-10 / lupus nephritis / RMT1-10 / Kim-1 |
Research Abstract |
The T-cell immunoglobulin mucin 1 (Tim-1), (Kim-1), modulates CD4+ T-cell responses and is also expressed by damaged proximal tubules. This study investigated the effects of an inhibitory anti-Tim-1 antibody (RMT1-10) in lupus-prone MRL-Faslpr mice. The mice were treated with RMT1-10 from 3 mo of age for 16 wk. RMT1-10 treatment significantly improved survival, limited the development of lymphadenopathy and skin lesions, preserved renal function and decreased proteinuria, reduced serum anti-DNA antibody levels, and attenuated renal leukocyte accumulation. Th1/Th17 cellular responses were reduced, but regulatory T/B cells were increased. RMT1-10 treatment also reduced glomerular immunoglobulin and C3 deposition and suppressed cellular proliferation and apoptosis. Urinary excretion and renal expression of Kim-1 was reduced, reflecting diminished interstitial injury. As RMT1-10 attenuated manipulating immune system Tim-1 may represent a therapeutic strategy in autoimmune diseases.
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Report
(3 results)
Research Products
(9 results)