Mammary tumor-derived CCL2 enhances pro-metastatic systemic inflammation through upregulation of IL1β in tumor-associated macrophages
Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we d...
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| Vydáno v: | Oncoimmunology Ročník 6; číslo 8; s. e1334744 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Taylor & Francis
03.08.2017
Taylor & Francis Group |
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| ISSN: | 2162-402X, 2162-4011, 2162-402X |
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| Abstract | Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of CCL2 positively correlates with IL1Β and macrophage markers in human breast tumors. We demonstrate that blockade of CCL2 in mammary tumor-bearing mice results in reduced IL17 production by γδ T cells, decreased neutrophil expansion and enhanced CD8
+
T cell activity. These results highlight a new role for CCL2 in facilitating the breast cancer-induced pro-metastatic systemic inflammatory γδ T cell - IL17 - neutrophil axis. |
|---|---|
| AbstractList | Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of CCL2 positively correlates with IL1Β and macrophage markers in human breast tumors. We demonstrate that blockade of CCL2 in mammary tumor-bearing mice results in reduced IL17 production by γδ T cells, decreased neutrophil expansion and enhanced CD8+ T cell activity. These results highlight a new role for CCL2 in facilitating the breast cancer-induced pro-metastatic systemic inflammatory γδ T cell – IL17 – neutrophil axis. Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of CCL2 positively correlates with IL1Β and macrophage markers in human breast tumors. We demonstrate that blockade of CCL2 in mammary tumor-bearing mice results in reduced IL17 production by γδ T cells, decreased neutrophil expansion and enhanced CD8 + T cell activity. These results highlight a new role for CCL2 in facilitating the breast cancer-induced pro-metastatic systemic inflammatory γδ T cell - IL17 - neutrophil axis. Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of positively correlates with and macrophage markers in human breast tumors. We demonstrate that blockade of CCL2 in mammary tumor-bearing mice results in reduced IL17 production by γδ T cells, decreased neutrophil expansion and enhanced CD8 T cell activity. These results highlight a new role for CCL2 in facilitating the breast cancer-induced pro-metastatic systemic inflammatory γδ T cell - IL17 - neutrophil axis. Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of CCL2 positively correlates with IL1Β and macrophage markers in human breast tumors. We demonstrate that blockade of CCL2 in mammary tumor-bearing mice results in reduced IL17 production by γδ T cells, decreased neutrophil expansion and enhanced CD8+ T cell activity. These results highlight a new role for CCL2 in facilitating the breast cancer-induced pro-metastatic systemic inflammatory γδ T cell - IL17 - neutrophil axis.Patients with primary solid malignancies frequently exhibit signs of systemic inflammation. Notably, elevated levels of neutrophils and their associated soluble mediators are regularly observed in cancer patients, and correlate with reduced survival and increased metastasis formation. Recently, we demonstrated a mechanistic link between mammary tumor-induced IL17-producing γδ T cells, systemic expansion of immunosuppressive neutrophils and metastasis formation in a genetically engineered mouse model for invasive breast cancer. How tumors orchestrate this systemic inflammatory cascade to facilitate dissemination remains unclear. Here we show that activation of this cascade relies on CCL2-mediated induction of IL1β in tumor-associated macrophages. In line with these findings, expression of CCL2 positively correlates with IL1Β and macrophage markers in human breast tumors. We demonstrate that blockade of CCL2 in mammary tumor-bearing mice results in reduced IL17 production by γδ T cells, decreased neutrophil expansion and enhanced CD8+ T cell activity. These results highlight a new role for CCL2 in facilitating the breast cancer-induced pro-metastatic systemic inflammatory γδ T cell - IL17 - neutrophil axis. |
| Author | Kersten, Kelly Coffelt, Seth B. Ciampricotti, Metamia Vrijland, Kim Hau, Cheei-Sing Salvagno, Camilla Wessels, Lodewyk F.A. Doshi, Parul Hoogstraat, Marlous Wellenstein, Max D. Lips, Esther H. de Visser, Karin E. Verstegen, Niels J.M. Doornebal, Chris W. |
| Author_xml | – sequence: 1 givenname: Kelly surname: Kersten fullname: Kersten, Kelly organization: Division of Immunology, Netherlands Cancer Institute – sequence: 2 givenname: Seth B. surname: Coffelt fullname: Coffelt, Seth B. organization: Division of Immunology, Netherlands Cancer Institute – sequence: 3 givenname: Marlous orcidid: 0000-0002-4916-1177 surname: Hoogstraat fullname: Hoogstraat, Marlous organization: Division of Molecular Carcinogenesis, Netherlands Cancer Institute – sequence: 4 givenname: Niels J.M. surname: Verstegen fullname: Verstegen, Niels J.M. organization: Division of Immunology, Netherlands Cancer Institute – sequence: 5 givenname: Kim surname: Vrijland fullname: Vrijland, Kim organization: Division of Immunology, Netherlands Cancer Institute – sequence: 6 givenname: Metamia surname: Ciampricotti fullname: Ciampricotti, Metamia organization: Division of Immunology, Netherlands Cancer Institute – sequence: 7 givenname: Chris W. surname: Doornebal fullname: Doornebal, Chris W. organization: Department of Anesthesiology, Academic Medical Center – sequence: 8 givenname: Cheei-Sing orcidid: 0000-0002-4728-4886 surname: Hau fullname: Hau, Cheei-Sing organization: Division of Immunology, Netherlands Cancer Institute – sequence: 9 givenname: Max D. surname: Wellenstein fullname: Wellenstein, Max D. organization: Division of Immunology, Netherlands Cancer Institute – sequence: 10 givenname: Camilla surname: Salvagno fullname: Salvagno, Camilla organization: Division of Immunology, Netherlands Cancer Institute – sequence: 11 givenname: Parul orcidid: 0000-0002-5399-5844 surname: Doshi fullname: Doshi, Parul organization: Janssen Research and Development – sequence: 12 givenname: Esther H. surname: Lips fullname: Lips, Esther H. organization: Division of Molecular Pathology, Netherlands Cancer Institute – sequence: 13 givenname: Lodewyk F.A. surname: Wessels fullname: Wessels, Lodewyk F.A. organization: Department of EEMCS, Delft University of Technology – sequence: 14 givenname: Karin E. orcidid: 0000-0002-0293-868X surname: de Visser fullname: de Visser, Karin E. email: k.d.visser@nki.nl organization: Division of Immunology, Netherlands Cancer Institute |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28919995$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2017 The Author(s). Published with license by Taylor & Francis Group, LLC © Kelly Kersten, Seth B. Coffelt, Marlous Hoogstraat, Niels J.M. Verstegen, Kim Vrijland, Metamia Ciampricotti, Chris W. Doornebal, Cheei-Sing Hau, Max D. Wellenstein, Camilla Salvagno, Parul Doshi, Esther H. Lips, Lodewyk F.A. Wessels, and Karin E. de Visser 2017 2017 The Author(s). Published with license by Taylor & Francis Group, LLC 2017 The Author(s) |
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| Keywords | γδ T cells tumor-induced inflammation CCL2 immunosuppression Breast cancer neutrophils tumor-associated macrophages |
| Language | English |
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| SubjectTerms | Breast cancer CCL2 immunosuppression neutrophils Original Research tumor-associated macrophages tumor-induced inflammation γδ T cells |
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| Title | Mammary tumor-derived CCL2 enhances pro-metastatic systemic inflammation through upregulation of IL1β in tumor-associated macrophages |
| URI | https://www.tandfonline.com/doi/abs/10.1080/2162402X.2017.1334744 https://www.ncbi.nlm.nih.gov/pubmed/28919995 https://www.proquest.com/docview/1940191051 https://pubmed.ncbi.nlm.nih.gov/PMC5593698 https://doaj.org/article/caf49ccdba7f4bf4a3af322e5ee3f07c |
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