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M2 macrophages and regulatory T cells in lethal prostate cancer
Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.ORCID-id: 0000-0001-5533-7899
Department of Medical Biosciences, Umeå University, Umeå, Sweden.
School of Medical Sciences, Örebro University, Örebro, Sweden. (Clinical Epidemiology and Biostatistics)
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2019 (engelsk)Inngår i: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 79, nr 4, s. 363-369Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

BACKGROUND: Prostate cancer (PCa) is one of the most frequently diagnosed cancers in the world. Emerging evidence suggests that inflammatory cells such as M2 macrophages and regulatory T cells (Tregs) can contribute to cancer progression by suppressing the anti‐tumor immune response. This study investigated the number of CD163‐positive M2 macrophages in PCa tissue. It also investigated the correlation and interaction of M2 macrophages and Tregs.

METHODS: were assessed using Spearman's rank-order correlation and a likelihood test, respectively. Logistic regression was used to estimate odds ratios (ORs) for lethal PCa and macrophage counts.

RESULTS: showed a significant correlation (P < 0.001) but no interactions. The OR for lethal PCa was 1.93 (95%CI: 1.23-3.03) for men with high numbers of M2 macrophages. Also for cases with uncertain outcome (GS categories 3 + 4 and 4 + 3) high numbers of M2 macrophages does predict a poorer prognosis.

CONCLUSIONS: Our data showed that men with high numbers of M2 macrophages in the prostate tumor environment had increased odds of dying of PCa. It is possible that M2 macrophages, together with other suppressor cells such as Tregs , promote an immunosuppressive environment.

sted, utgiver, år, opplag, sider
John Wiley & Sons, 2019. Vol. 79, nr 4, s. 363-369
Emneord [en]
CD163, FOXP3, TAMs, Tregs
HSV kategori
Identifikatorer
URN: urn:nbn:se:oru:diva-70404DOI: 10.1002/pros.23742ISI: 000456214000004PubMedID: 30500076Scopus ID: 2-s2.0-85057833977OAI: oai:DiVA.org:oru-70404DiVA, id: diva2:1267564
Tilgjengelig fra: 2018-12-03 Laget: 2018-12-03 Sist oppdatert: 2019-02-05bibliografisk kontrollert

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