Insulitis in transgenic mice expressing tumor necrosis factor beta (lymphotoxin) in the pancreas

Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10036-40. doi: 10.1073/pnas.89.21.10036.

Abstract

Tumor necrosis factor beta (TNF-beta) (lymphotoxin) may play an important role in the immune response and pathologic inflammatory diseases. Insulitis is an important early step in the development of insulin-dependent diabetes mellitus. To understand better the role of TNF-beta in the regulation of inflammation and type 1 diabetes, we produced transgenic mice in which the murine TNF-beta gene was regulated by the rat insulin II promoter. The transgene was expressed in the pancreas, kidney, and skin of transgenic mice. The expression of TNF-beta in the pancreas of transgenic mice resulted in a leukocytic inflammatory infiltrate consisting primarily of B220+ IgM+ B cells and CD4+ and CD8+ T cells. The insulitis is reminiscent of the early stages of diabetes, though the mice did not progress to diabetes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blotting, Northern
  • Insulin / biosynthesis
  • Islets of Langerhans / metabolism*
  • Islets of Langerhans / pathology
  • Lymphotoxin-alpha / biosynthesis*
  • Lymphotoxin-alpha / genetics*
  • Mice
  • Mice, Transgenic
  • Pancreas / metabolism*
  • Pancreas / pathology
  • Pancreatic Diseases / genetics*
  • Pancreatic Diseases / pathology
  • RNA / genetics
  • RNA / isolation & purification
  • RNA, Messenger / genetics
  • RNA, Messenger / isolation & purification
  • RNA, Messenger / metabolism
  • Rats
  • Restriction Mapping

Substances

  • Insulin
  • Lymphotoxin-alpha
  • RNA, Messenger
  • RNA