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Newtonian cell interactions shape natural killer cell education
KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics. Karolinska Inst, Microbiol Tumor & Cell Biol.ORCID iD: 0000-0001-5178-7593
2015 (English)In: Immunological Reviews, ISSN 0105-2896, E-ISSN 1600-065X, Vol. 267, no 1, 197-213 p.Article, review/survey (Refereed) Published
Abstract [en]

Newton's third law of motion states that for every action on a physical object there is an equal and opposite reaction. The dynamic change in functional potential of natural killer (NK) cells during education bears many features of such classical mechanics. Cumulative physical interactions between cells, under a constant influence of homeostatic drivers of differentiation, lead to a reactive spectrum that ultimately shapes the functionality of each NK cell. Inhibitory signaling from an array of self-specific receptors appear not only to suppress self-reactivity but also aid in the persistence of effector functions over time, thereby allowing the cell to gradually build up a functional potential. Conversely, the frequent non-cytolytic interactions between normal cells in the absence of such inhibitory signaling result in continuous stimulation of the cells and attenuation of effector function. Although an innate cell, the degree to which the fate of the NK cell is predetermined versus its ability to adapt to its own environment can be revealed through a Newtonian view of NK cell education, one which is both chronological and dynamic. As such, the development of NK cell functional diversity is the product of qualitatively different physical interactions with host cells, rather than simply the sum of their signals or an imprint based on intrinsically different transcriptional programs.

Place, publisher, year, edition, pages
2015. Vol. 267, no 1, 197-213 p.
Keyword [en]
natural killer cells, major histocompatibility complex, repertoire development, cytotoxicity, differentiation, cell surface molecules
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URN: urn:nbn:se:kth:diva-173423DOI: 10.1111/imr.12325ISI: 000360082000013PubMedID: 26284479ScopusID: 2-s2.0-84939533391OAI: diva2:853794

QC 20150915

Available from: 2015-09-15 Created: 2015-09-11 Last updated: 2015-09-15Bibliographically approved

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