Key result
Non-obese diabetic mice exhibit abnormal bone marrow markers and deficient myeloid progenitor cytokine responses.
Why the study?
Abnormalities in phenotype, cytokine responses, and function of myeloid lineage cells in NOD mice suggest bone marrow defects that may contribute to autoimmunity.
May indicate early hematopoietic defects in NOD autoimmunity; leaves open human relevance and clinical translation.
Several lines of evidence point to abnormalities of the phenotype, cytokine responses, and function of cells of the myeloid lineage in non-obese diabetic (NOD) mice. In this study we have characterized the phenotype and myeloid progenitor function of NOD bone marrow. Two hematopoietic differentiation antigens, Ly-6C and AA4.1, are expressed abnormally on NOD bone marrow cells. While multilineage erythromyeloid progenitor cells (day 12 CFU-S) are normal in number in NOD mice, more differentiated myeloid progenitors are deficient in their in vitro responses to IL-3, granulocyte/macrophage colony-stimulating factor (GM-CSF), and IL-5. Since the diabetes-predisposing Idd-5 gene of NOD mice maps close to the IL-1 receptor, we tested NOD bone marrow cells for a defect in synergy between IL-1 and IL-3; no defect was found. The defects in myelopoiesis described here may predispose the NOD mouse to autoimmunity by impairing macrophage maturation.
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Langmuir et al. (1993) studied Non-obese diabetic (NOD) mouse model. Non-obese diabetic (NOD) genotype was evaluated on Phenotype and myeloid progenitor function of bone marrow cells. Non-obese diabetic mice exhibit abnormal expression of Ly-6C and AA4.1 on bone marrow cells and deficient in vitro responses of differentiated myeloid progenitors to IL-3, GM-CSF, and IL-5.
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