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- Title
Administration of recombinant human thioredoxin-1 significantly delays and prevents autoimmune diabetes in nonobese diabetic mice through modulation of autoimmunity.
- Authors
Chernatynskaya, Anna V.; Looney, Benjamin; Hu, Hanbo; Zhu, Xiaoyan; Xia, Chang-Qing
- Abstract
Background Thioredoxin as a biological antioxidant plays an important role in regulating the redox system. The administration of recombinant thioredoxin has been demonstrated to be anti-inflammatory. In this study, the effect of recombinant human thioredoxin-1 (rhTrx-1) in preventing type 1 diabetes (T1D) in nonobese diabetic (NOD) mice was evaluated. Methods Eight-week-old NOD mice were treated with intravenous injection of rhTrx-1 (5 µg/mouse/day) for 5 weeks (5 days a week), followed by every other day for additional 5 weeks. Diabetes onset was monitored twice a week. Pancreatic histology and β-cell mass were examined by hematoxylin and eosin (H&E) and insulin immunohistochemistry staining, respectively. Adoptive transfer experiments were executed to assess autoimmune T cells modulated by rhTrx treatment. Results The intravenous administration of rhTrx-1 significantly delayed and prevented T1D in NOD mice. The histology data showed that rhTrx-1 treatment markedly reduced insulitic lesions and significantly preserved insulin-producing β cells. Adoptive transfer of spleen cells from rhTrx-1-treated mice into nonobese diabetic-severe combined immunodeficiency (NOD-SCID) mice significantly reduced the diabetes onset than transfer of those from phosphate-buffered saline-treated mice. Adoptive co-transfer experiments demonstrated that spleen cells from rhTrx-1-treated mice significantly delayed diabetes induced by the co-transferred diabetogenic spleen cells from the new-onset diabetic mice. Conclusions Antioxidant rhTrx-1 effectively prevents T1D which may be attributed to its activity to modulate autoimmunity. Copyright © 2011 John Wiley & Sons, Ltd.
- Publication
Diabetes/Metabolism Research & Reviews, 2011, Vol 27, Issue 8, p809
- ISSN
1520-7552
- Publication type
Article
- DOI
10.1002/dmrr.1232