Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF)

Similarities between TNF-α and interleukin

Chaim O. Jacob, Sadakazu Aiso, Sara A. Michie, Hugh O. Mcdevitt, Hans Acha-Orbea

Research output: Contribution to journalArticle

336 Citations (Scopus)

Abstract

The role of tumor necrosis factor α (TNF-α) in the pathogenesis of autoimmune diabetes mellitus was tested in the nonobese mouse (NOD) model system. The effects of TNF-α were assessed on three levels: (i) insulitis development, (ii) development of overt diabetes, (iii) adoptive transfer of diabetes by splenic lymphocytes. Spontaneous diabetes mellitus was blocked in NOD mice by long-term treatment with recombinant TNF-α. Treatment with TNF-α caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Class II major histocompatibility complex la expression by islet cells was not up-regulated by TNF-α. Moreover, TNF-α was able to suppress the induction of diabetes in adoptive transfer of lymphocytes from diabetic female mice to young nondiabetic male NOD mice. These activities of TNF-α were shared by interleukin 1α in this system. These studies have implications for the pathogenesis and therapy of autoimmune diabetes mellitus.

Original languageEnglish
Pages (from-to)968-972
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number3
DOIs
Publication statusPublished - 1990 Jan 1
Externally publishedYes

Keywords

  • Adoptive transfer
  • Autoimmune disease
  • Ia expression
  • Insulitis

ASJC Scopus subject areas

  • General

Cite this

Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF) : Similarities between TNF-α and interleukin. / Jacob, Chaim O.; Aiso, Sadakazu; Michie, Sara A.; Mcdevitt, Hugh O.; Acha-Orbea, Hans.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 87, No. 3, 01.01.1990, p. 968-972.

Research output: Contribution to journalArticle

@article{0d96f82d4a474e3585a8c17ba88d5730,
title = "Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): Similarities between TNF-α and interleukin",
abstract = "The role of tumor necrosis factor α (TNF-α) in the pathogenesis of autoimmune diabetes mellitus was tested in the nonobese mouse (NOD) model system. The effects of TNF-α were assessed on three levels: (i) insulitis development, (ii) development of overt diabetes, (iii) adoptive transfer of diabetes by splenic lymphocytes. Spontaneous diabetes mellitus was blocked in NOD mice by long-term treatment with recombinant TNF-α. Treatment with TNF-α caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Class II major histocompatibility complex la expression by islet cells was not up-regulated by TNF-α. Moreover, TNF-α was able to suppress the induction of diabetes in adoptive transfer of lymphocytes from diabetic female mice to young nondiabetic male NOD mice. These activities of TNF-α were shared by interleukin 1α in this system. These studies have implications for the pathogenesis and therapy of autoimmune diabetes mellitus.",
keywords = "Adoptive transfer, Autoimmune disease, Ia expression, Insulitis",
author = "Jacob, {Chaim O.} and Sadakazu Aiso and Michie, {Sara A.} and Mcdevitt, {Hugh O.} and Hans Acha-Orbea",
year = "1990",
month = "1",
day = "1",
doi = "10.1073/pnas.87.3.968",
language = "English",
volume = "87",
pages = "968--972",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "3",

}

TY - JOUR

T1 - Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF)

T2 - Similarities between TNF-α and interleukin

AU - Jacob, Chaim O.

AU - Aiso, Sadakazu

AU - Michie, Sara A.

AU - Mcdevitt, Hugh O.

AU - Acha-Orbea, Hans

PY - 1990/1/1

Y1 - 1990/1/1

N2 - The role of tumor necrosis factor α (TNF-α) in the pathogenesis of autoimmune diabetes mellitus was tested in the nonobese mouse (NOD) model system. The effects of TNF-α were assessed on three levels: (i) insulitis development, (ii) development of overt diabetes, (iii) adoptive transfer of diabetes by splenic lymphocytes. Spontaneous diabetes mellitus was blocked in NOD mice by long-term treatment with recombinant TNF-α. Treatment with TNF-α caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Class II major histocompatibility complex la expression by islet cells was not up-regulated by TNF-α. Moreover, TNF-α was able to suppress the induction of diabetes in adoptive transfer of lymphocytes from diabetic female mice to young nondiabetic male NOD mice. These activities of TNF-α were shared by interleukin 1α in this system. These studies have implications for the pathogenesis and therapy of autoimmune diabetes mellitus.

AB - The role of tumor necrosis factor α (TNF-α) in the pathogenesis of autoimmune diabetes mellitus was tested in the nonobese mouse (NOD) model system. The effects of TNF-α were assessed on three levels: (i) insulitis development, (ii) development of overt diabetes, (iii) adoptive transfer of diabetes by splenic lymphocytes. Spontaneous diabetes mellitus was blocked in NOD mice by long-term treatment with recombinant TNF-α. Treatment with TNF-α caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Class II major histocompatibility complex la expression by islet cells was not up-regulated by TNF-α. Moreover, TNF-α was able to suppress the induction of diabetes in adoptive transfer of lymphocytes from diabetic female mice to young nondiabetic male NOD mice. These activities of TNF-α were shared by interleukin 1α in this system. These studies have implications for the pathogenesis and therapy of autoimmune diabetes mellitus.

KW - Adoptive transfer

KW - Autoimmune disease

KW - Ia expression

KW - Insulitis

UR - http://www.scopus.com/inward/record.url?scp=0025020303&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025020303&partnerID=8YFLogxK

U2 - 10.1073/pnas.87.3.968

DO - 10.1073/pnas.87.3.968

M3 - Article

VL - 87

SP - 968

EP - 972

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 3

ER -