Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.molimm.2007.09.010
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dc.titleHarnessing the tumour-derived cytokine, CSF-1, to co-stimulate T-cell growth and activation
dc.contributor.authorLo, A.S.Y.
dc.contributor.authorTaylor, J.R.
dc.contributor.authorFarzaneh, F.
dc.contributor.authorKemeny, D.M.
dc.contributor.authorDibb, N.J.
dc.contributor.authorMaher, J.
dc.date.accessioned2016-12-13T05:36:45Z
dc.date.available2016-12-13T05:36:45Z
dc.date.issued2008-03
dc.identifier.citationLo, A.S.Y., Taylor, J.R., Farzaneh, F., Kemeny, D.M., Dibb, N.J., Maher, J. (2008-03). Harnessing the tumour-derived cytokine, CSF-1, to co-stimulate T-cell growth and activation. Molecular Immunology 45 (5) : 1276-1287. ScholarBank@NUS Repository. https://doi.org/10.1016/j.molimm.2007.09.010
dc.identifier.issn01615890
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/132806
dc.description.abstractAberrant growth factor production is a prevalent mechanism in tumourigenesis. If T-cells responded positively to a cancer-derived cytokine, this might result in selective enhancement of function within the tumour microenvironment. Here, we have chosen colony-stimulating factor-1 (CSF-1) as a candidate to test this concept. CSF-1 is greatly overproduced in many cancers but has no direct effects upon T-lymphocytes, which do not express the c-fms-encoded CSF-1 receptor. To confer CSF-1-responsiveness, we have expressed the human c-fms gene in immortalized and primary T-cells. Addition of soluble CSF-1 resulted in synergistic enhancement of IL-2-driven T-cell proliferation. CSF-1 also co-stimulated the production of interferon (IFN)-γ by activated T-cells. These effects required Y809 of the CSF-1R and activation of the Ras-MEK-MAP kinase cascade, but were independent of PI3K signalling. T-cells that express c-fms are also responsive to membrane-anchored CSF-1 (mCSF-1) which, unlike its soluble counterpart, could co-stimulate IL-2 production. CSF-1 promoted chemotaxis of c-fms-expressing primary human T-cells and greatly augmented proliferation mediated by a tumour-targeted chimeric antigen receptor, with preservation of tumour cytolytic activity. Taken together, these data establish that T-cells may be genetically modified to acquire responsiveness to CSF-1 and provide proof-of-principle for a novel strategy to enhance the effectiveness of adoptive T-cell immunotherapy. © 2007 Elsevier Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.molimm.2007.09.010
dc.sourceScopus
dc.subjectAdoptive immunotherapy
dc.subjectc-fms
dc.subjectCSF-1
dc.subjectT-cell
dc.typeArticle
dc.contributor.departmentMICROBIOLOGY
dc.description.doi10.1016/j.molimm.2007.09.010
dc.description.sourcetitleMolecular Immunology
dc.description.volume45
dc.description.issue5
dc.description.page1276-1287
dc.description.codenIMCHA
dc.identifier.isiut000253030000009
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