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Cited by 1,648

The DOI matches its Crossref record; 212 of the 212 references it cites were found in a registry or an index.

NK CELL RECEPTORS

Lanier, Lewis L.·1998·Annual Review of Immunology

Abstract

▪ Abstract NK cells are regulated by opposing signals from receptors that activate and inhibit effector function. While positive stimulation may be initiated by an array of co-stimulatory receptors, specificity is provided by inhibitory signals transduced by receptors for MHC class I. Three distinct receptor families, Ly49, CD94/NKG2, and KIR, are involved in NK cell recognition of polymorphic MHC class I molecules. A common pathway of inhibitory signaling is provided by ITIM sequences in the cytoplasmic domains of these otherwise structurally diverse receptors. Upon ligand binding and activation, the inhibitory NK cell receptors become tyrosine phosphorylated and recruit tyrosine phosphatases, SHP-1 and possibly SHP-2, resulting in inhibition of NK cell–mediated cytotoxicity and cytokine expression. Recent studies suggest these inhibitory NK cell receptors are members of a larger superfamily containing ITIM sequences, the inhibitory receptor superfamily (IRS).

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Crossref · 10.1146/annurev.immunol.16.1.359

Cites

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Citations

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Metadata

Authors
Lanier, L. L.
Venue
Annual Review of Immunology
Published
1998-04
Volume
16
Issue
1
Pages
359-393
ISSN
  • 0732-0582 (ISSN-L)
  • 1545-3278
OpenAlex
W2160520392
Cited by
1,648
References
212
FWCI
13.35
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: NK CELL RECEPTORS. https://app.cochat.ai/papers/10.1146/annurev.immunol.16.1.359
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Lanier, L. L. (1998). NK CELL RECEPTORS. Annual Review of Immunology. https://doi.org/10.1146/annurev.immunol.16.1.359

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.