Abstract
Type 1 diabetes (T1D) is characterized by a cellular infiltrate in pancreatic islets where β cells are destroyed. The recognition of antigens and auto antigens takes place by macrophages (Mo) and dendritic cells (DCs). Previously we have showed that MIF favors the expression of co-stimulatory molecules on Mo and DCs on infection diseases. However, the role of MIF on Mo and CDs in T1D has not been explored. Here, we determined the expression of co-stimulatory molecules on Mo and CDs from WT or MIF-/- mice on experimental T1D induced by STZ. Cells extracted from pancreas and spleens were treated with antibodies anti- CD80, CD86, CD40, MHC-II and TLRs. Also we tested the number of CD4+CD25+FOXp3+ cells. The results show that MIF-/- mice not developed high glucose levels compared with WT mice. Pro-inflammatory cytokines in serum were diminished on MIF-/-STZ mice, while the anti-inflammatory cytokines were higher compared to WT STZ mice. Moreover, MIF-/-STZ mice had less CD80, CD86, MHCII, TLR-2 and TLR-4 in spleen and pancreatic islets Mo and CDs. In addition, CD4+CD25+ spleen cells had a high expression of FOXp3 transcription factor in MIF-/- healthy than MIF+/+ healthy mice. 8 weeks after of STZ induction the MIF-/-STZ mice present higher FOXp3 expression than WT STZ mice. Our results suggest that MIF favors the expression of co-stimulatory molecules in the Mo and CDs in T1D. Additionally we propose that MIF down-regulate the proliferation of regulatory T cells in T1D.
- Copyright © 2013 by The American Association of Immunologists, Inc.
In this issue
