Abstract
Galectin 3 (Gal-3) is an antiapoptotic and a proinflammatory lectin. We hypothesized that the proinflammatory properties of Gal-3 may influence disease induction in the multiple low doses of streptozotocin model of diabetes. Diabetes was induced in C57BL/6 Gal-3+/+ and Gal-3-/- mice and disease monitored by blood glucose level, immuno-histology, insulin content of islets and expression of the proinflammatory cytokines, TNF-α, IFN-γ, IL-17, and iNOS in pancreatic lymph nodes. Gal-3+/+ mice developed delayed and sustained hyperglycemia, mononuclear cellular infiltration and reduced insulin content of islets accompanied with expression of proinflammatory cytokines. Gal-3-/- mice were relatively resistant to diabetogenesis as evaluated by glycemia, quantitative histology and insulin content. Further, we observed the weaker expression of IFN-γ and complete absence of TNF-α, and IL-17 in draining pancreatic lymph nodes. Macrophages, the first cells that infiltrate the islet in this model of diabetes, produce less TNF-α and NO in Gal-3-/- mice. Thus, Gal-3 is involved in immune mediated β cell damage and is required for diabetogenesis in this model of disease.
Original language | English (US) |
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Pages (from-to) | 83-88 |
Number of pages | 6 |
Journal | Clinical Immunology |
Volume | 130 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2009 |
Keywords
- Autoimmunity;
- Inducible nitric oxide synthase;
- Interferon-gamma;
- Interleukin-17
- Proinflammatory cytokines;
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy