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

M. O'Keefe, T.C. Brodnicki, B. Fancke, D. Vremec, Grant Morahan, E. Maraskovsky, R. Steptoe, L.C. Harrison, K. Shortman

Research output: Contribution to journalArticlepeer-review

49 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)307-314
JournalInternational Immunology
Volume17
Issue number3
DOIs
Publication statusPublished - 2005

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