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International Immunology Advance Access originally published online on January 31, 2005
International Immunology 2005 17(3):307-314; doi:10.1093/intimm/dxh210
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Featured Article of the Month

Fms-like tyrosine kinase 3 ligand administration overcomes a genetically determined dendritic cell deficiency in NOD mice and protects against diabetes development

Meredith O'Keeffe1, Thomas C. Brodnicki1, Ben Fancke1, David Vremec1, Grant Morahan1, Eugene Maraskovsky2, Raymond Steptoe1, Leonard C. Harrison1 and Ken Shortman1

1 Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia
2 Ludwig Institute for Cancer Research, Melbourne Tumour Biology Branch, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australia

Correspondence to: K. Shortman; E-mail: shortman{at}wehi.edu.au

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.

Keywords: autoimmune disease, dendritic cells, diabetes, Flt-3 ligand

Transmitting editor: A. Kelso


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