The Journal of Immunology, 2007, 178: 130.38.
Copyright © 2007 by The American Association of Immunologists, Inc.
Galectin 3 is required for MLD-STZ induced diabetes in mice
Miodrag L Lukic1,
Ahmed - Al-Hakim1,
Eric - Mensah-Brown2,
Daniel K Hsu3 and
Allen - Shahin1
1 Microbiology and Immunology,
2 Anatomy, Faculty of Medicine & Health Sciences, UAE University, Tawam Medical Campus, P O Box 17666, Al Ain, United Arab Emirates,
3 Dermatology, University of California, Davis, School of Medicine, Sacramento, Davis, California, CA 95817
Abstract
Galectin-3, member of ancient lectin family characterized by specific binding of 
galactosides, has an antiapoptotic function in T cells, macrophages and islet cells. It was therefore of interest to evaluate the susceptibility to multiple low dose induced diabetes (MLD-STZ) in galectin (gal-3) deficient C57BL/6 mice. Gal-3 –/– and gal-3+/+ mice were treated with 5 daily injections of 40 mg/kg STZ and diabetes development evaluated by glycemia and immunohistochemistry of the pancreas. Gal-3+/+ mice developed delayed sustained and progressive hyperglucemia and mononuclear cell infiltrates in the islets. Gal-3 –/– demonstrated only mild glycemia with minimal islet pathology as evaluated by the number of infiltrating cells and insulin content. There was higher number of apoptotic cells in the islets of galectin-3 knock out than in the control gal-3+/+ mice. RT PCR analysis of pancreatic lymph node cells 17 days after diabetes induction revealed the presence of IL-23 and IL-17 in gal-3+/+ but not in Gal-3 –/– mice. TNF-
and INF-
INOS expression was also attenuated in Gal-3 –/– mice. We concluded that antiapoptotic effect of gal-3 in diabetogenic cells favors the induction of disease. The data are also compatible with our previous finding that IL-23-Th17 axis plays a role in diabetogenesis (Eur J Immunol, 36: 216–23, 2006[Medline]).
(Supported by Sheikh Hamdan Awards for Medical Research).
