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Clin Immunol. 2013 Dec;149(3):432-9. doi: 10.1016/j.clim.2013.09.003. Epub 2013 Sep 14.

A selective role of NKG2D in inflammatory and autoimmune diseases.

Author information

1
Department of Molecular and Cell Biology, and Cancer Research Laboratory, 489 Life Sciences, Addition, University of California at Berkeley, Berkeley, CA 94720, USA.
2
Department of Life Science, Imperial College London, Imperial College Road, SW7 2AZ, London.
#
Contributed equally

Abstract

The NKG2D activating receptor has been implicated in numerous autoimmune diseases. We tested the role of NKG2D in models of autoimmunity and inflammation using NKG2D knockout mice and antibody blockade experiments. The severity of experimental autoimmune encephalitis (EAE) was decreased in NKG2D-deficient mice when the disease was induced with a limiting antigen dose, but unchanged with an optimal antigen dose. Surprisingly, however, NKG2D deficiency had no detectable effect in several other models, including two models of type 1 diabetes, and a model of intestinal inflammation induced by poly(I:C). NKG2D antibody blockade in normal mice also failed to inhibit disease in the NOD diabetes model or the intestinal inflammation model. Published evidence using NKG2D knockout mice demonstrated a role for NKG2D in mouse models of atherosclerosis and liver inflammation, as well as in chronic obstructive pulmonary disease. Therefore, our results suggest that NKG2D plays selective roles in inflammatory diseases.

KEYWORDS:

EAE; Intestinal inflammation; NK cells; NKG2D; NOD; Natural Killer Group 2, member D; Natural Killer cells; RAE-1; Retinoic Acid Early Inducible Gene-1; Type 1 diabetes; poly(I:C); polyinosinic:polycytidylic acid.

PMID:
24211717
PMCID:
PMC3868205
DOI:
10.1016/j.clim.2013.09.003
[Indexed for MEDLINE]
Free PMC Article

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