Fms-like tyrosine kinase 3 ligand administration overcomes a genetically determined dendritic cell deficiency in NOD mice and protects against diabetes development
- Author(s)
- O'Keeffe, M; Brodnicki, TC; Fancke, B; Vremec, D; Morahan, G; Maraskovsky, E; Steptoe, R; Harrison, LC; Shortman, K;
- Details
- Publication Year 2005-03,Volume 17,Issue #3,Page 307-314
- Journal Title
- INTERNATIONAL IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- OXFORD UNIV PRESS
- Keywords
- CD4 T-CELLS; IN-VIVO; FLT3 LIGAND; BIOLOGICAL-ACTIVITY; INTERLEUKIN (IL)-4; IFN-GAMMA; MOUSE; TOLERANCE; SUBSETS; CD8(+)
- Publisher's Version
- https://doi.org/10.1093/intimm/dxh210
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2005-03-01 12:00:00