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] |
|
Copyright of International Immunology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder