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Verfasst von:Mamidi, Srinivas [VerfasserIn]   i
 Höne, Simon [VerfasserIn]   i
 Kirschfink, Michael [VerfasserIn]   i
Titel:The complement system in cancer
Titelzusatz:ambivalence between tumour destruction and promotion
Verf.angabe:Srinivas Mamidi, Simon Höne, Michael Kirschfink
Jahr:2017
Jahr des Originals:2015
Umfang:10 S.
Fussnoten:Available online 28 November 2015 ; Gesehen am 07.09.2018
Titel Quelle:Enthalten in: Immunobiology
Ort Quelle:München : Elsevier, 1979
Jahr Quelle:2017
Band/Heft Quelle:222(2017), 1, Seite 45-54
ISSN Quelle:1878-3279
Abstract:Constituting a part of the innate immune system, the complement system consists of over 50 proteins either acting as part of a 3-branch activation cascade, a well-differentiated regulatory system in fluid phase or on each tissue, or as receptors translating the activation signal to multiple cellular effector functions. Complement serves as first line of defence against infections from bacteria, viruses and parasites by orchestrating the immune response through opsonisation, recruitment of immune cells to the site of infection and direct cell lysis. Complement is generally recognised as a protective mechanism against the formation of tumours in humans, but is often limited by various resistance mechanisms interfering with its cytotoxic action, now considered as a great barrier of successful antibody-based immunotherapy. However, recent studies also indicate a pro-tumourigenic potential of complement in certain cancers and under certain conditions. In this review, we present recent findings on the possible dual role of complement in destroying cancer, especially if resistance mechanisms are blocked, but also under certain inflammatory conditions—promoting tumour development.
DOI:doi:10.1016/j.imbio.2015.11.008
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: http://dx.doi.org/10.1016/j.imbio.2015.11.008
 Volltext: http://www.sciencedirect.com/science/article/pii/S0171298515300929
 DOI: https://doi.org/10.1016/j.imbio.2015.11.008
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:C3a
 C5a
 Cancer
 Complement regulatory proteins
 Complement-dependent cytotoxicity
 Opsonisation
K10plus-PPN:1580782256
Verknüpfungen:→ Zeitschrift

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