NKG2D blockade prevents autoimmune diabetes in NOD mice

Kouetsu Ogasawara, Jessica A. Hamerman, Lauren R. Ehrlich, Helene Bour-Jordan, Pere Santamaria, Jeffrey A. Bluestone, Lewis L. Lanier

Research output: Contribution to journalArticle

241 Citations (Scopus)

Abstract

NKG2D is an activating receptor on CD8+ T cells and NK cells that has been implicated in immunity against tumors and microbial pathogens. Here we show that RAE-1 is present in prediabetic pancreas islets of NOD mice and that autoreactive CD8+ T cells infiltrating the pancreas express NKG2D. Treatment with a nondepleting anti-NKG2D monoclonal antibody (mAb) during the prediabetic stage completely prevented disease by impairing the expansion and function of autoreactive CD8+ T cells. These findings demonstrate that NKG2D is essential for disease progression and suggest a new therapeutic target for autoimmune type I diabetes.

Original languageEnglish
Pages (from-to)757-767
Number of pages11
JournalImmunity
Volume20
Issue number6
DOIs
Publication statusPublished - 2004 Jun 1
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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  • Cite this

    Ogasawara, K., Hamerman, J. A., Ehrlich, L. R., Bour-Jordan, H., Santamaria, P., Bluestone, J. A., & Lanier, L. L. (2004). NKG2D blockade prevents autoimmune diabetes in NOD mice. Immunity, 20(6), 757-767. https://doi.org/10.1016/j.immuni.2004.05.008