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    Primary breast tumours but not lung metastases induce protective anti-tumour immune responses after Treg-depletion

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    Authors
    Hughes, Ellyn
    Lauder, S. N.
    Smart, K.
    Bloom, A.
    Scott, J.
    Jones, E.
    Somerville, M.
    Browne, M.
    Blainey, A.
    Godkin, A.
    Ager, A.
    Gallimore, A.
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    Affiliation
    Division of Infection and Immunity, Cardiff University School of Medicine, SIURI, Cardiff, CF14 4XN, UK.
    Issue Date
    2020
    
    Metadata
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    Abstract
    Although metastatic disease is responsible for the majority of cancer deaths, tests of novel immunotherapies in mouse tumour models often focus on primary tumours without determining whether these therapies also target metastatic disease. This study examined the impact of depleting Foxp3(+) regulatory T cells (Treg), on lung metastases, using a mouse model of breast cancer. After Treg-depletion, generation of an immune response to the primary tumour was a critical determinant for limiting development of metastasis. Indeed, resection of the primary tumour abrogated any effect of Treg-depletion on metastases. In addition, whilst the immune response, generated by the primary tumour, prevented metastases development, it had little impact on controlling established disease. Collectively, the data indicate that metastatic cells in the lung are not controlled by immune responses induced by the primary tumour. These findings indicate that targeting Tregs alone will not suffice for treating lung metastases.
    Citation
    E. Hughes, S. N. Lauder, K. Smart et al. Primary breast tumours but not lung metastases induce protective anti-tumour immune responses after Treg-depletion. Cancer Immunol Immunother. 2020.
    Journal
    Cancer Immunology Immunotherapy
    URI
    http://hdl.handle.net/10541/623055
    DOI
    10.1007/s00262-020-02603-x
    PubMed ID
    32447412
    Additional Links
    https://dx.doi.org/10.1007/s00262-020-02603-x
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1007/s00262-020-02603-x
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