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Cited by 258

The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.

Cutting Edge: Induction of IFN-γ Production but Not Cytotoxicity by the Killer Cell Ig-Like Receptor KIR2DL4 (CD158d) in Resting NK Cells

Rajagopalan, Sumati, Fu, Jacqueline, Long, Eric O·2001·The Journal of Immunology

Abstract

Activated NK cells lyse tumor cells and virus-infected cells and produce IFN-γ upon contact with sensitive target cells. The regulation of these effector responses in resting NK cells is not well understood. We now describe a receptor, KIR2DL4, that has the unique property of inducing IFN-γ production, but not cytotoxicity, by resting NK cells in the absence of cytokines. In contrast, the NK cell-activation receptors CD16 and 2B4 induced cytotoxicity but not IFN-γ production. The induction by KIR2DL4 of IFN-γ production by resting NK cells was blocked by an inhibitor of the p38 mitogen-activated protein kinase signaling pathway, in contrast to the IL-2-induced IFN-γ secretion that was sensitive to inhibition of the extracellular signal-regulated kinase mitogen-activated protein kinase pathway. These results reveal a functional dichotomy (cytokine production vs cytotoxicity) in the response of resting NK cells, as dictated by the signals of individual receptors.

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Metadata

Authors
Rajagopalan, S., Fu, J., & Long, E. O.
Venue
The Journal of Immunology
Published
2001-08
Volume
167
Issue
4
Pages
1877-1881
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W1931291333
Cited by
258
References
21
FWCI
7.33
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Cutting Edge: Induction of IFN-γ Production but Not Cytotoxicity by the Killer Cell Ig-Like Receptor KIR2DL4 (CD158d) in Resting NK Cells. https://app.cochat.ai/papers/10.4049/jimmunol.167.4.1877
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Rajagopalan, S., Fu, J., & Long, E. O. (2001). Cutting Edge: Induction of IFN-γ Production but Not Cytotoxicity by the Killer Cell Ig-Like Receptor KIR2DL4 (CD158d) in Resting NK Cells. The Journal of Immunology. https://doi.org/10.4049/jimmunol.167.4.1877

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