| First Author | O'Keeffe M | Year | 2005 |
| Journal | Int Immunol | Volume | 17 |
| Issue | 3 | Pages | 307-14 |
| PubMed ID | 15684037 | Mgi Jnum | J:96315 |
| Mgi Id | MGI:3530163 | Doi | 10.1093/intimm/dxh210 |
| Citation | O'keeffe M, et al. (2005) Fms-like tyrosine kinase 3 ligand administration overcomes a genetically determined dendritic cell deficiency in NOD mice and protects against diabetes development. Int Immunol 17(3):307-14 |
| abstractText | A dendritic cell (DC) imbalance with a marked deficiency in CD4(-)8(+) DC occurs in non-obese diabetic (NOD) mice, a model of human autoimmune diabetes mellitus. Using a NOD congenic mouse strain, we find that this CD4(-)8(+) DC deficiency is associated with a gene segment on chromosome 4, which also encompasses non-MHC diabetes susceptibility loci. Treatment of NOD mice with fms-like tyrosine kinase 3 ligand (FL) enhances the level of CD4(-)8(+) DC, temporarily reversing the DC subtype imbalance. At the same time, fms-like tryosine kinase 3 ligand treatment blocks early stages of the diabetogenic process and with appropriately timed administration can completely prevent diabetes development. This points to a possible clinical use of FL to prevent autoimmune disease. |
