NK CELL RECOGNITION

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Abstract

The integrated processing of signals transduced by activating and inhibitory cell surface receptors regulates NK cell effector functions. Here, I review the structure, function, and ligand specificity of the receptors responsible for NK cell recognition.

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HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C.

V Braud, D. Allan, C A O'Callaghan … (1998)

The protein HLA-E is a non-classical major histocompatibility complex (MHC) molecule of limited sequence variability. Its expression on the cell surface is regulated by the binding of peptides derived from the signal sequence of some other MHC class I molecules. Here we report the identification of ligands for HLA-E. We constructed tetramers in which recombinant HLA-E and beta2-microglobulin were refolded with an MHC leader-sequence peptide, biotinylated, and conjugated to phycoerythrin-labelled Extravidin. This HLA-E tetramer bound to natural killer (NK) cells and a small subset of T cells from peripheral blood. On transfectants, the tetramer bound to the CD94/NKG2A, CD94/NKGK2B and CD94/NKG2C NK cell receptors, but did not bind to the immunoglobulin family of NK cell receptors (KIR). Surface expression of HLA-E was enough to protect target cells from lysis by CD94/NKG2A+ NK-cell clones. A subset of HLA class I alleles has been shown to inhibit killing by CD94/NKG2A+ NK-cell clones. Only the HLA alleles that possess a leader peptide capable of upregulating HLA-E surface expression confer resistance to NK-cell-mediated lysis, implying that their action is mediated by HLA-E, the predominant ligand for the NK cell inhibitory receptor CD94/NKG2A.

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In search of the ‘missing self’: MHC molecules and NK cell recognition

Hans-Gustaf Ljunggren, Klas Kärre (1990)

Immunology Today, 11, 237-244

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Selective rejection of H-2-deficient lymphoma variants suggests alternative immune defence strategy.

K Kärre, H G Ljunggren, G Piontek … (1986)

Metazoan organisms may discriminate between self and non-self not only by the presence of foreign antigens but also by the absence of normal self markers. Mammalian adaptive immune responses use the first strategy, with the additional requirement that foreign antigens are recognized in the context of self-major histocompatibility complex (MHC) products at the cell surface. Aberrant cells which fail to express MHC products adequately can therefore avoid detection. A more primitive but complementary defence system, eliminating such cells on the basis of absent self-markers, is suggested by a re-interpretation of phenomena associated with metastasis and natural resistance. We now show that murine lymphoma cells selected for loss of H-2 expression are less malignant after low-dose inoculation in syngeneic hosts than are wild-type cells, and that the rejection of such cells is non-adaptive. On the basis of our data, we suggest that natural killer cells are effector cells in a defence system geared to detect the deleted or reduced expression of self-MHC.

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Author and article information

Journal

Title: Annual Review of Immunology

Abbreviated Title: Annu. Rev. Immunol.

Publisher: Annual Reviews

ISSN (Print): 0732-0582

ISSN (Electronic): 1545-3278

Publication date Created: April 2005

Publication date (Print): April 2005

Volume: 23

Issue: 1

Pages: 225-274

Affiliations

[1 ]Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco School of Medicine, San Francisco, California 94143-0414; email:

Article

DOI: 10.1146/annurev.immunol.23.021704.115526

PubMed ID: 15771571

SO-VID: 317c10d4-d2bb-4867-8619-69469c86945d

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