| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2081990 | Drug Discovery Today: Disease Mechanisms | 2006 | 6 Pages |
Loss of insulin secretory function and ultimately destruction of the beta cells themselves, are prerequisites for transition into the diabetic state. Considerable evidence indicates that the cytotoxic action of proinflammatory cytokines on pancreatic islets in vitro is mediated through intra-beta cell free radical generation. Yet, it is unclear in vivo how these cytokines act to promote beta cell destruction. We propose that in vivo combinations of proinflammatory mediators serve to predispose beta cells for lysis by autoreactive cytotoxic T lymphocytes subsequent to the lesion that initiates the disease.
Section editors:John Corbett – Saint Louis University School of Medicine, Saint Louis, USAClayton Mathews – University of Pittsburgh School of Medicine, Pittsburgh, USA
