The Journal of Immunology, 2007, 178: 129.36.
Copyright © 2007 by The American Association of Immunologists, Inc.
Il-23 enhances diabetes induction in the wild type but not in INF-gamma –/– mice
Miodrag L Lukic1,
Allen - Shahin1,
Eric - Mensah-Brown2 and
Ahmed - Al-Hakim2
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
Abstract
C57BL/6 male mice developed delayed progressive and sustained hyperglucemia, insulitis and loss of 
cells when injected with 5 (40 µg/ kg b/w) daily doses of streptozotocin (STZ). C57BL/6 INF-
–/– mice treated with same regimen develop the disease at the later stage (by day 28) but reach the same level of functional impairment by day 52 after disease induction. RT PCR analysis of the pancreatic lymph nodes revealed the presence of TNF, INF-, and IL-17 and in the "wild type" mice and only TNF-
and IL-17 in INF- –/– mice. Four injections of STZ did not induce hyperglycemia neither in the "wild type" nor INF- –/– mice. Concomitant treatment with IL-23 (10 x 40 mg/daily) dramatically enhanced the effect of this subdiabetogenic treatment in "wild type" mice, accompanied with the expression of TNF, INF- and IL-17 in the pancreatic lymph node while INF- –/– mice did not develop disease. We assume that INF- is required for the initial activation of antigen presenting cells in suboptimal conditions for diabetes induction but not for the expansion and activation of effector cells in this model of toxin induce autoimmune diabetes which is IL-23-IL-17 dependent (European Journal of Immunology, 36: 216–23, 2006[Medline]).
