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Secreted Factors from Colorectal and Prostate Cancer Cells Skew the Immune Response in Opposite Directions.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umeå, Sweden.ORCID iD: 0000-0002-8306-0687
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2015 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 5, article id 15651Article in journal (Refereed) Published
Abstract [en]

Macrophage infiltration has been associated with an improved prognosis in patients with colorectal cancer (CRC), but a poor prognosis in prostate cancer (PC) patients. In this study, the distribution and prognostic value of proinflammatory M1 macrophages (NOS2(+)) and immunosuppressive M2 macrophages (CD163(+)) was evaluated in a cohort of 234 PC patients. We found that macrophages infiltrating PC were mainly of an M2 type and correlated with a more aggressive tumor and poor patient prognosis. Furthermore, the M1/M2 ratio was significantly decreased in PC compared to CRC. Using in vitro cell culture experiments, we could show that factors secreted from CRC and PC cells induced macrophages of a proinflammatory or immunosuppressive phenotype, respectively. These macrophages differentially affected autologous T lymphocyte proliferation and activation. Consistent with this, CRC specimens were found to have higher degrees of infiltrating T-helper 1 cells and active cytotoxic T lymphocytes, while PC specimens displayed functionally inactive T cells. In conclusion, our results imply that tumour-secreted factors from cancers of different origin can drive macrophage differentiation in opposite directions and thereby regulate the organization of the anti-tumour immune response. Our findings suggest that reprogramming of macrophages could be an important tool in the development of new immunotherapeutic strategies.

Place, publisher, year, edition, pages
2015. Vol. 5, article id 15651
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Cancer and Oncology
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URN: urn:nbn:se:uu:diva-349308DOI: 10.1038/srep15651PubMedID: 26503803OAI: oai:DiVA.org:uu-349308DiVA, id: diva2:1201368
Funder
Swedish Cancer SocietySwedish Research CouncilAvailable from: 2018-04-25 Created: 2018-04-25 Last updated: 2018-05-17Bibliographically approved

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