@article{ebc51be95d6740de89e6cf1960a4bb69,
title = "NKG2D blockade prevents autoimmune diabetes in NOD mice",
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.",
author = "Kouetsu Ogasawara and Hamerman, {Jessica A.} and Ehrlich, {Lauren R.} and Helene Bour-Jordan and Pere Santamaria and Bluestone, {Jeffrey A.} and Lanier, {Lewis L.}",
note = "Funding Information: We thank Greg Szot for expert assistance with islet cell isolation, Tadashi Nishiya for expert assistance with the microscopy, and B. Seaman, J. Ryan, and all Bluestone and Lanier lab members for technical assistance and critical discussion. A Pilot & Feasibility grant from the UCSF DERC # P60 DK63720, NIH grant CA89189, and JDRFI Center Grant 4-1999-841 supported this work. A Human Frontier Science Program Long-Term Fellowship supports K.O., J.A.H is an Irvington Foundation Fellow, L.R.E is funded by a fellowship from the Damon Runyon Cancer Research Foundation, and L.L.L. is an American Cancer Society Research Professor. P.S. is supported by the Canadian Institutes of Health Research and is a Scientist of the Alberta Heritage Foundation for Medical Research. ",
year = "2004",
month = jun,
doi = "10.1016/j.immuni.2004.05.008",
language = "English",
volume = "20",
pages = "757--767",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "6",
}