Transgenic mice have a diphtheria toxin (DT) inducible system that transiently depletes macrophages. The transgene insert contains a fusion product involving simian diphtheria toxin receptor (HBEGF) and green fluorescent protein under the control of the human ITGAM (integrin alpha M) promoter (CD11b). RT-PCR analysis of bone marrow macrophages detects specific transgene expression. Cytological analysis of thioglycollate treated peritoneal cells shows the absence of macrophages. Intraperitoneal injection of DT ablates monocyte/macrophage cells in the peritoneal cavity. Unmanipulated CD11b/DTR NOD mice are viable, normal in size and develop spontaneous diabetes similar to NOD/ShiLtJ. Transgene expression of EGFP is not sufficient to be detected by FACS analysis. Twelve hours following DT administration all macrophages are ablated in the spleen and lymph nodes, including the pancreatic lymph node and pancreas for three to five days. Macrophage population is restored by day four following a single intraperitoneal dose of DT. Administration of DT does not affect polymorphonuclear cells. DT treated CD11b-DTR/NOD.scid mice and controls used in diabetes transfer studies became diabetic by days 10-14. Higher doses (greater than 25ng/g body weight) of DT sickens the mice. Transgene expression is not sufficient to be detected by FACS analysis. This mutant mouse strain may be useful in studies of the specific role of macrophages in the immune response, specifically in the context of type 1 diabetes.

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These congenic NOD mice are hemizygous for a transgene encoding a simian diphtheria toxin receptor (HBEGF) fused with green fluorescent protein under the control of human integrin alpha M, ITGAM, promoter (CD11b). These transgenic mice provide a diphtheria toxin inducible system that transiently depletes macrophages. This transgenic strain is useful for studying the specific role of macrophages in the immune response, specifically in the context of type 1 diabetes.

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