GENETIC REQUIREMENTS FOR ACCELERATION OF DIABETES IN NONOBESE DIABETIC MICE EXPRESSING INTERLEUKIN-2 IN ISLET BETA-CELLS
- Author(s)
- Allison, J; McClive, P; Oxbrow, L; BAXTER, A; Morahan, G; Miller, JFAP;
- Details
- Publication Year 1994-10,Volume 24,Issue #10,Page 2535-2541
- Journal Title
- EUROPEAN JOURNAL OF IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- Diabetes was dramatically accelerated in non-obese diabetic (NOD) transgenic mice that expressed interleukin-2 (IL-2) in their beta cells. A single cross to C57BL/6 completely prevented this effect and a further backcross to the NOD genetic background showed that at least two diabetes susceptibility loci (Idd1s and Idd3/10s) were required for the diabetes acceleration. T cells activated to islet antigens were not circulating in the mice. The accelerating effect of IL-2 was present, but decreased, in NOD mice that lacked CD8(+) T cells as well as in NOD SCID mice. The implications are that in the NOD genetic background, the production of cytokines, such as IL-2, by islet-specific CD4(+) T cells can lead to beta cell damage and diabetes and that CD8(+) T cells may have a role in accelerating diabetes onset.
- Publisher
- VCH PUBLISHERS INC
- Keywords
- CD8+ T-CELLS; NECROSIS-FACTOR-ALPHA; TRANSGENIC MICE; VIRUS-INFECTION; MOUSE STRAINS; INSULITIS; CD4+; DESTRUCTION; MELLITUS; AUTOIMMUNITY
- Publisher's Version
- https://doi.org/10.1002/eji.1830241041
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1994-10-01 12:00:00