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Altering macrophage polarization in the tumor environment: the role of response gene to complement 32

Cellular & Molecular Immunology volume 12, pages 783–784 (2015)Cite this article

In a study reported in this issue, Zhao et al.6 evaluated the expression and role of response gene to complement 32 (RGC-32) in macrophages and tumor-associated macrophages (TAMs). First, they demonstrated that both a cultured macrophage-like cell line and monocyte-derived macrophages up-regulated RGC-32 when exposed to either IL-4 or macrophage colony-stimulating factor. Other products and genes associated with M2/heal-type macrophages were also upregulated, whereas the products associated with M1/inhibit-type macrophages were downregulated. RGC-32 thus appears to be a good marker for M2-type macrophage activity.

Zhao et al.6 further showed that ascites tumor fluid enhanced RGC-32 and M2-type cytokines, in accordance with the evidence that either tumors or tumor-associated cells can produce factors that decrease the M1/M2 ratio and inhibit effective antitumor activity.

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Authors and Affiliations

  1. Clinica di Oncologia Medica, AOU Ospedali Riuniti, Università Politecnica delle Marche, Ancona, Italy

    Matteo Santoni & Stefano Cascinu

  2. BioMedical Consultants, Marine on St. Croix, MN, USA

    Charles D Mills

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  1. Matteo Santoni
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  2. Stefano Cascinu
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  3. Charles D Mills
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Correspondence to Matteo Santoni.

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Santoni, M., Cascinu, S. & Mills, C. Altering macrophage polarization in the tumor environment: the role of response gene to complement 32. Cell Mol Immunol 12, 783–784 (2015). https://doi.org/10.1038/cmi.2014.115

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