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.

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.

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.

Antioxidant rhTrx‐1 effectively prevents T1D which may be attributed to its activity to modulate autoimmunity. Copyright © 2011 John Wiley & Sons, Ltd.