The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
LFA-1 Contributes an Early Signal for NK Cell Cytotoxicity
Abstract
Cytotoxicity of human NK cells is activated by receptors that bind ligands on target cells, but the relative contribution of the many different activating and inhibitory NK cell receptors is difficult to assess. In this study, we describe an experimental system that circumvents some of the difficulties. Adhesion through β2 integrin LFA-1 is a common requirement of CTLs and NK cells for efficient lysis of target cells. However, the contribution of LFA-1 to activation signals for NK cell cytotoxicity, besides its role in adhesion, is unclear. The role of LFA-1 was evaluated by exposing NK cells to human ICAM-1 that was either expressed on a Drosophila insect cell line, or directly coupled to beads. Expression of ICAM-1 on insect cells was sufficient to induce lysis by NK cells through LFA-1. Coexpression of peptide-loaded HLA-C with ICAM-1 on insect cells blocked the LFA-1-dependent cytotoxicity of NK cells that expressed HLA-C-specific inhibitory receptors. Polarization of cytotoxic granules in NK cells toward ICAM-1- and ICAM-2-coated beads showed that engagement of LFA-1 alone is sufficient to initiate activation signals in NK cells. Thus, in contrast to T cells, in which even adhesion through LFA-1 is dependent on signals from other receptors, NK cells receive early activation signals directly through LFA-1.
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Citations
Cites
Hynes (2002) · doi:10.1016/s0092-8674(02)00971-6 · Cited by 8,606
Activating Receptors and Coreceptors Involved in Human Natural Killer Cell-Mediated Cytolysis
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T-cell receptor cross-linking transiently stimulates adhesiveness through LFA-1
Dustin, M. L., & Springer, T. A. (1989) · Nature · doi:10.1038/341619a0 · Cited by 1,538
Takagi, J., Petre, B. M., Walz, T., & Springer, T. A. (2002) · Cell · doi:10.1016/s0092-8674(02)00935-2 · Cited by 1,168
Natural killer cells, viruses and cancer
Cerwenka, A., & Lanier, L. L. (2001) · Nature Reviews Immunology · doi:10.1038/35095564 · Cited by 875
Bidirectional Transmembrane Signaling by Cytoplasmic Domain Separation in Integrins
Kim, M., Carman, C. V., & Springer, T. A. (2003) · Science · doi:10.1126/science.1084174 · Cited by 786
Unravelling natural killer cell function: triggering and inhibitory human NK receptors
Moretta, L., & Moretta, A. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600019 · Cited by 615
Syk is required for integrin signaling in neutrophils
Mócsai, A., Zhou, M., Meng, F., Tybulewicz, V. L., & Lowell, C. A. (2002) · Immunity · doi:10.1016/s1074-7613(02)00303-5 · Cited by 421
NKG2D-DAP10 triggers human NK cell–mediated killing via a Syk-independent regulatory pathway
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On guard—activating NK cell receptors
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Cited by
Natural killer cells act as rheostats modulating antiviral T cells
Waggoner, S. N., Cornberg, M., Selin, L. K., & Welsh, R. M. (2012) · Nature · doi:10.1038/nature10624 · Cited by 607
Bryceson, Y. T., March, M. E., Barber, D. F., Ljunggren, H.-G., & Long, E. O. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20051143 · Cited by 515
Self-citationMukhtar, O., Dutt, R., Panda, A., Kumari, P., Singh, S. S., Paul, G., Prakash, N., Abbas, M., Islam, M. M., Arora, P., et al. (2026) · eLife · doi:10.7554/elife.110942
Mukhtar, O., Dutt, R., Panda, A., Kumari, P., Singh, S. S., Paul, G., Prakash, N., Abbas, M., Islam, M. M., Arora, P., et al. (2026) · eLife · doi:10.7554/elife.110942.3
Metadata
- Authors
- Barber, D. F., Faure, M., & Long, E. O.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-09
- Volume
- 173
- Issue
- 6
- Pages
- 3653-3659
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1669828090
- Cited by
- 321
- References
- 58
- FWCI
- 4.34
- Type
- journal article
- Language
- en
- Open access
- closed
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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).
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