التفاصيل البيبلوغرافية
العنوان: |
Fms-like tyrosine kinase 3 ligand administration overcomes a genetically determined dendritic cell deficiency in NOD mice and protects against diabetes development. |
المؤلفون: |
Meredith O'Keeffe, Thomas C. Brodnicki, Ben Fancke, David Vremec, Grant Morahan, Eugene Maraskovsky, Raymond Steptoe, Leonard C. Harrison, Ken Shortman |
المصدر: |
International Immunology; Mar2005, Vol. 17 Issue 3, p307-314, 8p |
مصطلحات موضوعية: |
DIABETIC acidosis, TYROSINE, ANTIGEN presenting cells, RODENTS |
مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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قاعدة البيانات: |
Complementary Index |