Research ArticleCancer

Disruption of CXCR2-Mediated MDSC Tumor Trafficking Enhances Anti-PD1 Efficacy

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Science Translational Medicine  21 May 2014:
Vol. 6, Issue 237, pp. 237ra67
DOI: 10.1126/scitranslmed.3007974

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  • RE: A combinatorial approach: the modulation of CXCR2-mediated MDSC tumour trafficking to enhance anti-PD1 checkpoint blockade

    To the Editor,

    I read with interest the article authored by Steven Highfill et al (1) and entitled: “Disruption of CXCR2-mediated MDSC tumour trafficking enhances anti-PD1 efficacy”.

    This article presented a series of studies that analysed the effectiveness of PD1 blockade on tumours utilising a mouse model of rhabdomyosarcoma (RMS) and that also examined the role of CXCR2-mediated trafficking of granulocytic and monocytic CXCR2+CD11b+Ly6Chigh myeloid-derived suppressor cells (MDSCs).

    Although it is accepted that checkpoint blockade has been a significant development towards improving immunotherapeutic anti-cancer therapies, that anti-PD1 remained ineffective against established tumours when compared with anti-PD1 treatment at the time of tumour inoculation highlighted an important constrain on its effectiveness that will be relevant to other settings.

    This work clearly showed that the ineffectiveness of delayed anti-PD1 blockade could be rescued by either CXCR2 deficiency or anti-CXCR2 monoclonal antibody therapy and it was demonstrated that the mechanism by which this was achieved in this context was by the prevention of CXCR2+CD11b+Ly6Hhigh MDSCs from moving to the tumour.

    In addition, that the granulocytic CXCR2+CD11b+Ly6Hhigh MDSCs were found to be the more suppressive subtype compared with monocytic CXCR2+CD11b+Ly6Hhigh MDSCs within this setting was also of interest.

    A set of elegant experiments and encouraging results that...

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    Competing Interests: None declared.

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