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https://hdl.handle.net/2440/43405
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dc.contributor.author | Simson, L. | - |
dc.contributor.author | Ellyard, J. | - |
dc.contributor.author | Dent, L. | - |
dc.contributor.author | Matthaei, K. | - |
dc.contributor.author | Rothenberg, M. | - |
dc.contributor.author | Foster, P. | - |
dc.contributor.author | Smyth, M. | - |
dc.contributor.author | Parish, C. | - |
dc.date.issued | 2007 | - |
dc.identifier.citation | Journal of Immunology, 2007; 178(7):4222-4229 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.issn | 1550-6606 | - |
dc.identifier.uri | http://hdl.handle.net/2440/43405 | - |
dc.description | Copyright © 2007 by The American Association of Immunologists, Inc. | - |
dc.description.abstract | 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 play a role in tumor immune surveillance by determining the incidence of methylcholanthrene (MCA)-induced fibrosarcomas in IL-5 transgenic mice that have greatly enhanced levels of circulating eosinophils, CCL11 (eotaxin-1)-deficient mice that lack a key chemokine that recruits eosinophils into tissues, and the eosinophil-deficient mouse strains, IL-5/CCL11(-/-) and DeltadblGATA. 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 eosinophil-deficient IL-5/CCL11(-/-) and DeltadblGATA 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.description.statementofresponsibility | Ljubov Simson, Julia I. Ellyard, Lindsay A. Dent, Klaus I. Matthaei, Marc E. Rothenberg, Paul S. Foster, Mark J. Smyth and Christopher R. Parish | - |
dc.language.iso | en | - |
dc.publisher | Amer Assoc Immunologists | - |
dc.source.uri | http://www.jimmunol.org/cgi/content/abstract/178/7/4222 | - |
dc.subject | Eosinophils | - |
dc.subject | Animals | - |
dc.subject | Mice, Transgenic | - |
dc.subject | Mice | - |
dc.subject | Neoplasms | - |
dc.subject | Fibrosarcoma | - |
dc.subject | Cell Transformation, Neoplastic | - |
dc.subject | Methylcholanthrene | - |
dc.subject | Chemokines, CC | - |
dc.subject | Interleukin-5 | - |
dc.subject | Immunologic Surveillance | - |
dc.subject | Male | - |
dc.subject | Chemokine CCL11 | - |
dc.title | Regulation of carcinogenesis by IL-5 and CCL11: A potential role for eosinophils in tumor immune surveillance | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.4049/jimmunol.178.7.4222 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Dent, L. [0000-0002-3521-408X] | - |
Appears in Collections: | Aurora harvest Molecular and Biomedical Science publications |
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