Islet-infiltrating T cell clones from non-obese diabetic mice that promote or prevent accelerated onset diabetes
✍ Scribed by Oleh Pankewycz; Terry B. Strom; Vicki E. Rubin-Kelley
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- English
- Weight
- 770 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Islet-infiltrating T cell clones from non-obese diabetic mice that promote or prevent accelerated onset diabetes*
In humans and non-obese diabetic mice (NOD), insulin-dependent diabetes mellitus (IDDM) results from a spontaneous T cell-dependent autoimmune destruction of insulin-producing pancreatic fJ cells. Previous data suggest that a delicate balance between autoaggressive T cells and suppressor-type immune phenomena determine whether expression of autoimmunity is limited to insulitis or progresses to IDDM. To resolve the cellular basis of this intricate network of pathogenic CD4+ and CD8+ Tcells and the role of Tcells in suppressive immune phenomena,Tcell clones were propagated directly from islets of NOD mice at the onset of insulitis. Insofar as insulitis, but not IDDM, is universal in NOD mice,we have screened for the in vivo effects of the islet-infiltrating Tcell clones upon expression of IDDM, not insulitis. A CD4+ Tcell clone, IS-3S7D, proliferates in response to islet antigen(s) and its transfer into prediabetic NOD mice promotes the rapid onset of IDDM. An interleukin 2 (IL 2)-dependent noncytolytic,Vgll+ CD8+,Tcell clone, IS-2.15, prevents an accelerated onset diabetes in two distinct models.The present study,which documents the presence of CD4+ diabetogenicT cell clones and CD8+ T cell clones that dampen autoimmunity, gives tangible evidence that opposing autoimmune processes may determine whether an autoimmune-prone host develops frank disease.