Sentence examples for free nod from inspiring English sources

To our surprise, the incidence of type-1 diabetes in female germ free NOD mice (n = 22) was indistinguishable from that of NOD mice housed under SPF conditions in our colony (n = 20) (Figure 1, p>0.6696) or the 80% incidence of female NOD mice housed under SPF conditions at Taconic (Figure 1, p<0.78).

Total splenocytes were recovered from 32-week-old diabetes-free NOD mice that have been treated with anti-GITRL antibody (from week 11 to 14 of life).

These findings challenge the view that germ-free NOD mice have increased diabetes incidence and demonstrate that modulation of intestinal microbiota can prevent the development of type-1 diabetes.

Our study suggests, for the first time, that CD4+CD25+ regulatory T cells may play an important role in the control of diabetogenic cells and prevention of diabetes development in CFA-treated disease-free NOD mice.

Total splenocytes were harvested from 32-week-old anti-GITRL antibody-treated diabetes-free NOD mice and were depleted of regulatory T cells i.e. CD4+CD25+ T cells and CD4+CD62L+ T cells [39] [41].

Taken together, these findings debunk the myth that germ-free NOD female mice have increased diabetes incidence and support the notion that modulation of intestinal microbiota can have beneficial effects on the development of autoimmune diabetes.

Mechanistically, the key role of innate immunity has been further supported by the recent report that genetic ablation of the key adaptor of innate immunity, MyD88, affords protection from T1D in specific pathogen-free NOD mice [15].

That from NOD mice is most likely inducing diabetes since the colonization of these mice with a microbiota from non-type 1 diabetic mice prevented the incidence of diabetes in germ-free NOD mice.

Gluten-free NOD mice had lower insulitis (P < 0·0001); reduced expression of NKG2D on DX5+ NK cells in spleen and auricular lymph nodes (P < 0·05); and on CD8+ T cells in pancreas-associated lymph nodes (P = 0·04).

Although the incidence of insulitis is not significantly different between germ-free and specific-pathogen-free (SPF) NOD mice, germ-free mice develop insulitis earlier than SPF mice [ 10, 11].

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