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TUMOUR IMMUNOLOGY

Enhancing antitumour eosinophils

Nature Reviews Immunology volume 19, pages 202–203 (2019)Cite this article

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One mechanism by which tumours can evade host immune responses is the perturbation of lymphocyte migration through the post-translational modification of chemokines. In this regard, increased expression of dipeptidyl peptidase 4 (DPP4; also known as CD26) has been observed in mouse and human tumours and is associated with worse survival. Twelve human chemokines have been validated as substrates of DPP4, including CXC-chemokine ligand 10 (CXCL10), cleavage of which limits T cell-mediated and natural killer (NK) cell-mediated antitumour responses. Matthew Albert and colleagues now describe that inhibition of DPP4 can improve antitumour immune responses by enhancing the effects of eosinophils.

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Original article

  • Hollande, C. et al. Inhibition of the dipeptidyl peptidase DPP4 (CD26) reveals IL-33-dependent eosinophil-mediated control of tumor growth. Nat. Immunol. 20, 257–264 (2019)

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  1. Nature Reviews Immunology http://www.nature.com/nri/

    Kirsty Minton

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  1. Kirsty Minton
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Correspondence to Kirsty Minton.

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Minton, K. Enhancing antitumour eosinophils. Nat Rev Immunol 19, 202–203 (2019). https://doi.org/10.1038/s41577-019-0142-7

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  • DOI: https://doi.org/10.1038/s41577-019-0142-7

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