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DPP4 in anti-tumor immunity: going beyond the enzyme

Nature Immunology volume 16, pages 791–792 (2015)Cite this article

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Effective anti-tumor immune therapy in solid tumors relies on the presence of effector T cells. Inhibition of the dipeptidylpeptidase DPP4 (CD26) enhances chemokine CXCL10–mediated infiltration of lymphocytes into the tumor parenchyma, which results in diminished tumor growth.

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Figure 1: Inhibition of DPP4 suppresses truncation of its ligand CXCL10, which leads to the recruitment of CXCR3+ T cells into tumor parenchyma.

Marina Corral Spence/Nature Publishing Group

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Authors and Affiliations

  1. Ryo Hatano and Chikao Morimoto are in the Department of Therapy Development and Innovation for Immune Disorders and Cancers, Kei Ohnuma, Graduate School of Medicine, Juntendo University, Tokyo, Japan.,

    Kei Ohnuma, Ryo Hatano & Chikao Morimoto

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  1. Kei Ohnuma
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  2. Ryo Hatano
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  3. Chikao Morimoto
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Correspondence to Chikao Morimoto.

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Ohnuma, K., Hatano, R. & Morimoto, C. DPP4 in anti-tumor immunity: going beyond the enzyme. Nat Immunol 16, 791–792 (2015). https://doi.org/10.1038/ni.3210

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