In vivo natural killer cell activities revealed by natural killer cell-deficient mice.

Abstract:

:Studies of natural killer (NK) cell function in vivo have been challenging primarily due to the lack of animal models in which NK cells are genetically and selectively deficient. Here, we describe a transgenic mouse with defective natural killing and selective deficiency in NK1.1(+) CD3(-) cells. Despite functionally normal B, T, and NK/T cells, transgenic mice displayed impaired acute in vivo rejection of tumor cells. Adoptive transfer experiments confirmed that NK1.1(+) CD3(-) cells were responsible for acute tumor rejection, establishing the relationship of NK1.1(+) CD3(-) cells to NK cells. Additional studies provided evidence that (i) NK cells play an important role in suppressing tumor metastasis and outgrowth; (ii) NK cells are major producers of IFNgamma in response to bacterial endotoxin but not to interleukin-12, and; (iii) NK cells are not essential for humoral responses to T cell-independent type 2 antigen or the generalized Shwartzman reaction, both of which were previously proposed to involve NK cells.

authors

Kim S,Iizuka K,Aguila HL,Weissman IL,Yokoyama WM

doi

10.1073/pnas.050588297

keywords:

subject

Has Abstract

pub_date

2000-03-14 00:00:00

pages

2731-6

issue

6

eissn

0027-8424

issn

1091-6490

pii

050588297

journal_volume

97

pub_type

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