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Verfasst von:Urlaub, Doris [VerfasserIn]   i
 Höfer, Kristine [VerfasserIn]   i
 Müller, Martha-Lena [VerfasserIn]   i
Titel:LFA-1 activation in NK cells and their subsets
Titelzusatz:influence of receptors, maturation, and cytokine stimulation
Verf.angabe:Doris Urlaub, Kristine Höfer, Martha-Lena Müller, and Carsten Watzl
E-Jahr:2017
Jahr:18 January 2017
Umfang:8 S.
Fussnoten:Gesehen am 15.10.2018
Titel Quelle:Enthalten in: The journal of immunology
Ort Quelle:Rockville, Md. : American Association of Immunologists, 1916
Jahr Quelle:2017
Band/Heft Quelle:198(2017), 5, Seite 1944-1951
ISSN Quelle:1550-6606
Abstract:The integrin LFA-1 is essential for efficient activation and for cytotoxicity of NK cells because it initiates the assembly of the immunological synapse and mediates firm adhesion to the target. LFA-1 is also needed to polarize the cytotoxic machinery of the NK cell toward the target cell. The binding affinity and avidity of integrins can be regulated via inside-out signals from other receptors. In this article, we investigate the signals necessary to activate LFA-1 in human NK cells. Our data show that LFA-1 has a low ligand-binding activity in resting human NK cells, but it can be stimulated by triggering activating receptors, such as 2B4 or CD16, or by coactivation of different receptor combinations. Short-term stimulation of freshly isolated NK cells with cytokines, such as IL-15, IL-12, or IL-18, does not activate LFA-1 but increases the responsiveness of the cells to subsequent receptor stimulation. Different NK cell subsets vary in their ability to induce LFA-1 binding activity after activating receptor stimulation. Interestingly, the NK cell subsets that are more mature and possess higher cytotoxic potential also show the highest activation of LFA-1, which correlated with the expression of the small calcium-binding protein S100A4. Our data suggest that regulation of LFA-1 is one reason for the different activity of NK cells during differentiation.
DOI:doi:10.4049/jimmunol.1601004
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: http://dx.doi.org/10.4049/jimmunol.1601004
 kostenfrei: Volltext: http://www.jimmunol.org/content/198/5/1944
 DOI: https://doi.org/10.4049/jimmunol.1601004
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1581894805
Verknüpfungen:→ Zeitschrift

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