Header

UZH-Logo

Maintenance Infos

Effector pathways of natural killer cells


Van den Broek, M F; Kägi, D; Hengartner, H (1998). Effector pathways of natural killer cells. Current topics in microbiology and immunology, 230:123-131.

Abstract

Cell-mediated cytotoxicity is an important mechanism of tumor control (Melief 1992) and virus elimination (Zinkemagel and Rosenthal 1981) in vivo. Depending on the tumor target, the host has two complementary cytotoxic mechanisms at its disposal: cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. NK cells are not antigen specific in the classical sense and can be activated within hours without specific priming. In contrast, CTLs are induced by specific peptides presented by major histocompatibility complex (MHC) class I molecules, are antigen-specific, and act efficiently as effector cells only after an induction and proliferation phase of 5–8 days. A tumor or an infected cell can prime acquired immunity if it presents tumor-specific peptides in the context of MHC class I and/or class II molecules to CD8+ or CD4+ T cells, respectively (Melief 1992; van Pel et al. 1995). Under selective pressure, however, tumors may escape immune surveillance by variants that lack MHC class I and/or II molecules (Schrier et al. 1983; Smith et al. 1989; Uyttenhove et al. 1983), and some of these tumors have been shown to be controlled efficiently by NK cells in vivo (Kärre et al. 1986, 1995). In addition, some viruses have been shown to use similar strategies to avoid immunological control: herpes simplex virus types 1 and 2 (Hill et al. 1994) and murine cytomegalovirus (del Val et al. 1992) downregulate MHC class I molecules upon infection, leaving only NK cells as effectors of cell-mediated cytotoxicity.

Abstract

Cell-mediated cytotoxicity is an important mechanism of tumor control (Melief 1992) and virus elimination (Zinkemagel and Rosenthal 1981) in vivo. Depending on the tumor target, the host has two complementary cytotoxic mechanisms at its disposal: cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. NK cells are not antigen specific in the classical sense and can be activated within hours without specific priming. In contrast, CTLs are induced by specific peptides presented by major histocompatibility complex (MHC) class I molecules, are antigen-specific, and act efficiently as effector cells only after an induction and proliferation phase of 5–8 days. A tumor or an infected cell can prime acquired immunity if it presents tumor-specific peptides in the context of MHC class I and/or class II molecules to CD8+ or CD4+ T cells, respectively (Melief 1992; van Pel et al. 1995). Under selective pressure, however, tumors may escape immune surveillance by variants that lack MHC class I and/or II molecules (Schrier et al. 1983; Smith et al. 1989; Uyttenhove et al. 1983), and some of these tumors have been shown to be controlled efficiently by NK cells in vivo (Kärre et al. 1986, 1995). In addition, some viruses have been shown to use similar strategies to avoid immunological control: herpes simplex virus types 1 and 2 (Hill et al. 1994) and murine cytomegalovirus (del Val et al. 1992) downregulate MHC class I molecules upon infection, leaving only NK cells as effectors of cell-mediated cytotoxicity.

Statistics

Citations

Dimensions.ai Metrics
5 citations in Web of Science®
8 citations in Scopus®
Google Scholar™

Altmetrics

Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Immunology and Allergy
Life Sciences > Microbiology
Life Sciences > Immunology
Health Sciences > Microbiology (medical)
Language:English
Date:1998
Deposited On:08 Feb 2018 15:03
Last Modified:11 Nov 2022 11:01
Publisher:Springer
ISSN:0070-217X
OA Status:Closed
Publisher DOI:https://doi.org/10.1007/978-3-642-46859-9_9
Official URL:https://link.springer.com/chapter/10.1007%2F978-3-642-46859-9_9.html
PubMed ID:9586354
Full text not available from this repository.