Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. NOD females homozygous for the Itgal mutation (commonly referred to as LFA1 or CD11a) remain normoglycemic to 34 weeks of age. Histological evaluation indicated the pancreatic islets were mostly normal, but some lymphocytic infiltrates were observed. Cd18, Cd11a and Cd49 expression are significantly reduced in splenic CD3 T-cells. Adoptive transfer experiments utilizing NOD-Rag1 mutant mice that received splenocytes from NOD-Itgal mutant mice did not become diabetic and no insulitis was observed. However, there were more leukocytes and CD3+ T-cells found than in control transfer experiments. 
NODShiLtJ mice carrying the Itgal mutation may be useful to further study the role of leukocyte intergrins in T-cell activation leading to insulitis and Type 1Diabetes.

This diabetes resistant congenic NOD.Itgal deficient mutant may be useful to further study the role of leukocyte intergrins in inflammatory disease models, specifically Type 1 Diabetes.

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