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Verfasst von:Kapp, Katharina [VerfasserIn]   i
 Langhans, Claus-Dieter [VerfasserIn]   i
Titel:Granulocyte functions are independent of arginine availability
Verf.angabe:Katharina Kapp, Steve Prüfer, Christian S. Michel, Alice Habermeier, Claudia Luckner‐Minden, Thomas Giese, John Bomalaski, Claus-Dieter Langhans, Pascale Kropf, Ingrid Müller, Ellen I. Closs, Markus P. Radsak, and Markus Munder
E-Jahr:2014
Jahr:07 August 2014
Umfang:7 S.
Fussnoten:Gesehen am 22.10.2020
Titel Quelle:Enthalten in: Journal of leukocyte biology
Ort Quelle:Hoboken, NJ : Wiley, 1984
Jahr Quelle:2014
Band/Heft Quelle:96(2014), 6, Seite 1047-1053
ISSN Quelle:1938-3673
Abstract:Arginine depletion via myeloid cell arginase is critically involved in suppression of the adaptive immune system during cancer or chronic inflammation. On the other hand, arginine depletion is being developed as a novel anti‐tumor metabolic strategy to deprive arginine‐auxotrophic cancer cells of this amino acid. In human immune cells, arginase is mainly expressed constitutively in PMNs. We therefore purified human primary PMNs from healthy donors and analyzed PMN function as the main innate effector cell and arginase producer in the context of arginine deficiency. We demonstrate that human PMN viability, activation‐induced IL‐8 synthesis, chemotaxis, phagocytosis, generation of ROS, and fungicidal activity are not impaired by the absence of arginine in vitro. Also, profound pharmacological arginine depletion in vivo via ADI‐PEG20 did not inhibit PMN functions in a mouse model of pulmonary invasive aspergillosis; PMN invasion into the lung, activation, and successful PMN‐dependent clearance of Aspergillus fumigatus and survival of mice were not impaired. These novel findings add to a better understanding of immunity during inflammation‐associated arginine depletion and are also important for the development of therapeutic arginine depletion as anti‐metabolic tumor therapy.
DOI:doi:10.1189/jlb.3AB0214-082R
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.

Volltext ; Verlag: https://doi.org/10.1189/jlb.3AB0214-082R
 Volltext: https://jlb.onlinelibrary.wiley.com/doi/abs/10.1189/jlb.3AB0214-082R
 DOI: https://doi.org/10.1189/jlb.3AB0214-082R
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:arginase
 immunosuppression
 innate immunity
 neutrophil
K10plus-PPN:1736246127
Verknüpfungen:→ Zeitschrift

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