Short term treatment with NCR1.15 down-regulates NKp46-mediated activity on pancreatic β-cells and inhibits LD-STZ induced diabetes.

<p>(A) Purified splenic NK cells from treated cells were co-incubated for 2–4 hours with purified C57BL/6 β-cells in the presence of anti-CD107a antibody. CD107a surface levels on NK cells were assessed by FACS. * <i>p</i><0.05 by Student's unpaired <i>t</i>-test. (B) LD-STZ induced diabetes development in C57BL/6 mice following 50μg injections at days-2 and 5. (<i>n</i> = 8). Animals were considered diabetic when blood glucose was ≥300mg/dl. *** <i>p</i><0.005 Kaplan-M log-rank (Mental-Cox). (C) Body weight of mice in the indicated groups following the LD-STZ administration; body weight baselines at day 0 of the control and NCR1.15 groups were 19.2±0.86, 19.8±1 grams, respectively. * <i>p</i><0.05, ** <i>p</i><0.01, *** <i>p</i><0.005 by Student's unpaired <i>t</i>-test. Bars, ±SD. (D) Representative H&E sections of the pancreas from sex&age-matched C57BL/6 mice treated with NCR1.15 or mock-treated (IgG1, κ) in LD-STZ induced diabetes model (magnification X40). (E) Summary of insulitis score over the days calculated as described in [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118936#pone.0118936.ref037" target="_blank">37</a>]. Score is quantified from 0 (low) to 4 (most severe).