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The Journal of Immunology, Vol 152, Issue 9 4407-4416, Copyright © 1994 by American Association of Immunologists
ARTICLES |
K Takeda, MW Moore and G Dennert
Department of Microbiology, Norris Comprehensive Cancer Center, University of Southern California School of Medicine, Los Angeles 90033.
The question of how irradiated mice acutely reject marrow grafts has remained controversial, and evidence in support of T cell- and natural killer cell-mediated rejection mechanisms has been provided. Here we show in support of previous data that CB17 severe combined immunodeficiency mice acutely reject allogeneic marrow but the specificity of rejection cannot be mapped within the MHC. It is shown that a similar rejection specificity is also expressed in normal CB17 mice and that it is caused by CD3- or CD3+ effector cells that do not utilize TCR. In search of TCR-independent rejection mechanisms in other mouse strains, use is made of TCR transgenic mice expressing a defect in recognizing H-2Dd. It is shown that, although marrow graft rejection is impaired in these mice, pointing to participation of TCR in the rejection process, residual resistance does exist. This resistance maps to the MHC, cannot be shown to involve TCR, and appears to be expressed by NK1+ CD3+ cells. It is concluded that acute marrow graft rejection in normal mice can be mediated by both TCR-mediated and NK cell receptor-dependent effector mechanisms, depending on the particular mouse strains.
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