Nature Immunology
6, 938 - 945 (2005)
Published online: 7 August 2005; | doi:10.1038/ni1236
Function of NKG2D in natural killer cell−mediated rejection of mouse bone marrow graftsKouetsu Ogasawara1, 2, Jonathan Benjamin1, Rayna Takaki1, 3, Joseph H Phillips4
& Lewis L Lanier11
Department of Microbiology & Immunology and the Cancer Research Institute, University of California, San Francisco, California 94143-0414, USA. 2
Department of Intractable Diseases, Division of Clinical Immunology, The Research Institute, International Medical Center of Japan, Toyama, Shinjuku-ku, Tokyo 162-8655, Japan. 3
Biomedical Sciences Graduate Program, University of California, San Francisco, California 94143-0414, USA. 4
Schering Plough BioPharma, Palo Alto, California 94304, USA.
Correspondence should be addressed to Lewis L Lanier lanier@itsa.ucsf.edu Irradiation-resistant natural killer (NK) cells in an F1 recipient can reject parental bone marrow, and host NK cells can also prevent engraftment of allogeneic bone marrow. We show here that repopulating bone marrow cells in certain mouse strains expressed retinoic acid early inducible 1 proteins, which are ligands for the activating NKG2D NK cell receptor. Treatment with a neutralizing antibody to NKG2D prevented rejection of parental BALB/c bone marrow in (C57BL/6  BALB/c) F1 recipients and allowed engraftment of allogeneic BALB.B bone marrow in C57BL/6 recipients. Additionally, bone marrow from C57BL/6 mice transgenic for retinoic acid early inducible 1 was rejected by syngeneic mice but was accepted after treatment with antibody to NKG2D. If other stem cells or tissues upregulate expression of NKG2D ligands after transplantation, NKG2D may contribute to graft rejection in immunocompetent hosts.
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