International Immunology, Vol 10, 785-790, Copyright © 1998 by Oxford University Press
M Bennett, PA Taylor, M Austin, MB Baker, LB Schook, M Rutherford, V Kumar, ER Podack, KM Mohler, RB Levy and BR Blazar
Mouse NK cells may use both cytokine, e.g. IFN-gamma, tumor necrosis factor
(TNF)-alpha and IL-12, and cytotoxic, e.g. perforin and Fas- FasL, pathways
to reject incompatible bone marrow cell (BMC) grafts. To begin a dissection
of these two major pathways, mice bearing deletional mutations of
IFN-gamma, TNF-RI/II or perforin, or mice treated with mAb to IL-12,
IFN-gamma or NK1.1 were irradiated and challenged with class I-deficient
BMC grafts, a system in which only NK cells are the effector cells.
Proliferation of the donor-derived cells was judged in terms of splenic
incorporation of [125I]iododeoxyuridine 5 or 7 days after cell transfer.
All of these mice maintained in a specific pathogen-free (s.p.f.)
environment were able to reject the BMC, except those treated with
anti-NK1.1 mAb. However, perforin deficient mice maintained in a
conventional breeding facility failed to reject class I (Tap-1)-deficient
marrow cells. Transfer of mice from the pathogen-free to the conventional
facility resulted in a slow and incomplete loss of the ability to reject
marrow cells. Thus, the breeding colony environment can elicit otherwise
undetectable defects in the rejection ability of perforin-deficient NK
cells. This report will hopefully alert those investigators who have only
studied immune gene knockout mice in s.p.f. facilities and found no
significant abnormalities.
ARTICLES
Cytokine and cytotoxic pathways of NK cell rejection of class I- deficient bone marrow grafts: influence of mouse colony environment
Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235, USA.
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