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Regulation of Carcinogenesis by IL-5 and CCL11: A Potential Role for Eosinophils in Tumor Immune Surveillance

Simson, Ljubov; Ellyard, Julia; Dent, Lindsay; Matthaei, Klaus; Rothenberg, Marc E; Foster, Paul S; Smyth, Mark J; Parish, Christopher

Description

The role of the immune system in the surveillance of transformed cells has seen a resurgence of interest in the last 10 years, with a substantial body of data in mice and humans supporting a role for the immune system in host protection from tumor development and in shaping tumor immunogenicity. A number of earlier studies have demonstrated that eosinophils, when recruited into tumors, can very effectively eradicate transplantable tumors. In this study, we investigated whether eosinophils also...[Show more]

dc.contributor.authorSimson, Ljubov
dc.contributor.authorEllyard, Julia
dc.contributor.authorDent, Lindsay
dc.contributor.authorMatthaei, Klaus
dc.contributor.authorRothenberg, Marc E
dc.contributor.authorFoster, Paul S
dc.contributor.authorSmyth, Mark J
dc.contributor.authorParish, Christopher
dc.date.accessioned2015-12-07T22:49:27Z
dc.identifier.issn0022-1767
dc.identifier.urihttp://hdl.handle.net/1885/26759
dc.description.abstractThe role of the immune system in the surveillance of transformed cells has seen a resurgence of interest in the last 10 years, with a substantial body of data in mice and humans supporting a role for the immune system in host protection from tumor development and in shaping tumor immunogenicity. A number of earlier studies have demonstrated that eosinophils, when recruited into tumors, can very effectively eradicate transplantable tumors. In this study, we investigated whether eosinophils also play a role in tumor immune surveillance by determining the incidence of methylcholanthrene (MCA)-induced flbrosarcomas in IL-5 transgenic mice that have greatly enhanced levels of circulating eosinophils, CCL11 (eotaxin-l)-deficient mice that lack a key chemokine that recruits eosinophils into tissues, and the eosinophil-deficient mouse strains, IL-5/CCL11-/- and ΔdblGATA. It was found that MCA-induced tumor incidence and growth were significantly attenuated in IL-5 transgenic mice of both the BALB/c and C57BL/6 backgrounds. Histological examination revealed that the protective effect of IL-5 was associated with massively enhanced numbers of eosinophils within and surrounding tumors. Conversely, there was a higher tumor incidence in CCL11-/- BALB/c mice, which was associated with a reduced eosinophil influx into tumors. This correlation was confirmed in the eosinephil-deficient IL-5/CCL11-/- and ΔdblGATA mouse strains, where tumor incidence was greatly increased in the total absence of eosinophils. In addition, subsequent in vitro studies found that eosinophils could directly kill MCA-induced fibrosarcoma cells. Collectively, our data support a potential role for the eosinophil as an effector cell in tumor immune surveillance.
dc.publisherAmerican Association of Immunologists
dc.sourceJournal of Immunology
dc.subjectKeywords: 3 methylcholanthrene; eotaxin; interleukin 5; animal cell; animal experiment; animal model; animal tissue; article; Bagg albino mouse; C57BL mouse; cancer immunology; carcinogenesis; cell transformation; controlled study; effector cell; eosinophil; fibros
dc.titleRegulation of Carcinogenesis by IL-5 and CCL11: A Potential Role for Eosinophils in Tumor Immune Surveillance
dc.typeJournal article
local.description.notesImported from ARIES
local.identifier.citationvolume178
dc.date.issued2007
local.identifier.absfor110709 - Tumour Immunology
local.identifier.ariespublicationu6800332xPUB46
local.type.statusPublished Version
local.contributor.affiliationSimson, Ljubov, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationEllyard, Julia, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationDent, Lindsay, University of Adelaide
local.contributor.affiliationMatthaei, Klaus, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationRothenberg, Marc E, University of Cincinnati
local.contributor.affiliationFoster, Paul S, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationSmyth, Mark J, Peter MacCallum Cancer Centre
local.contributor.affiliationParish, Christopher, College of Medicine, Biology and Environment, ANU
local.description.embargo2037-12-31
local.bibliographicCitation.startpage4222
local.bibliographicCitation.lastpage4229
dc.date.updated2015-12-07T12:08:46Z
local.identifier.scopusID2-s2.0-33947689316
CollectionsANU Research Publications

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