Clec9A + Dendritic Cells Are Not Essential for Antitumor CD8 + T Cell Responses Induced by Poly I:C Immunotherapy

In the steady state, tumors harbor several populations of dendritic cells (DCs) and myeloid cells that are key regulators of the intratumoral immune environment. Among these cells, migratory CD103 cross-presenting DCs are thought to be critical for tumor-specific CTL responses and tumor resistance....

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Published inThe Journal of immunology (1950) Vol. 200; no. 8; pp. 2978 - 2986
Main Authors Gilfillan, Connie B, Kuhn, Sabine, Baey, Camille, Hyde, Evelyn J, Yang, Jianping, Ruedl, Christiane, Ronchese, Franca
Format Journal Article
LanguageEnglish
Published United States American Association of Immunologists 15.04.2018
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Abstract In the steady state, tumors harbor several populations of dendritic cells (DCs) and myeloid cells that are key regulators of the intratumoral immune environment. Among these cells, migratory CD103 cross-presenting DCs are thought to be critical for tumor-specific CTL responses and tumor resistance. However, it is unclear whether this prominent role also extends to immunotherapy. We used a murine orthotopic mammary tumor model, as well as Clec9A-diphtheria toxin receptor mice that can be depleted of the specialized cross-presenting CD8α and CD103 DC1 subsets, to investigate the role of these DCs in immunotherapy. Treatment with monosodium urate crystals and mycobacteria at the tumor site delayed tumor growth and required DC1s for efficacy. In contrast, treatment with poly I:C was equally effective regardless of DC1 depletion. Neither treatment affected myeloid-derived suppressor cell numbers in the spleen or tumor. Similar experiments using subcutaneous B16 melanoma tumors in BATF3-knockout mice confirmed that CD103 DCs were not necessary for successful poly I:C immunotherapy. Nevertheless, adaptive immune responses were essential for the response to poly I:C, because mice depleted of CD8 T cells or all DC subsets were unable to delay tumor growth. In vivo experiments showed that DC1 and DC2 subsets were able to take up tumor Ags, with DC2s making up the larger proportion of lymph node DCs carrying tumor material. Both DC subsets were able to cross-present OVA to OT-I T cells in vitro. Thus, immunotherapy with poly I:C enables multiple DC subsets to cross-present tumor Ag for effective antitumor immune responses.
AbstractList In the steady state, tumors harbor several populations of dendritic cells (DCs) and myeloid cells that are key regulators of the intratumoral immune environment. Among these cells, migratory CD103+ cross-presenting DCs are thought to be critical for tumor-specific CTL responses and tumor resistance. However, it is unclear whether this prominent role also extends to immunotherapy. We used a murine orthotopic mammary tumor model, as well as Clec9A–diphtheria toxin receptor mice that can be depleted of the specialized cross-presenting CD8α+ and CD103+ DC1 subsets, to investigate the role of these DCs in immunotherapy. Treatment with monosodium urate crystals and mycobacteria at the tumor site delayed tumor growth and required DC1s for efficacy. In contrast, treatment with poly I:C was equally effective regardless of DC1 depletion. Neither treatment affected myeloid-derived suppressor cell numbers in the spleen or tumor. Similar experiments using subcutaneous B16 melanoma tumors in BATF3-knockout mice confirmed that CD103+ DCs were not necessary for successful poly I:C immunotherapy. Nevertheless, adaptive immune responses were essential for the response to poly I:C, because mice depleted of CD8+ T cells or all DC subsets were unable to delay tumor growth. In vivo experiments showed that DC1 and DC2 subsets were able to take up tumor Ags, with DC2s making up the larger proportion of lymph node DCs carrying tumor material. Both DC subsets were able to cross-present OVA to OT-I T cells in vitro. Thus, immunotherapy with poly I:C enables multiple DC subsets to cross-present tumor Ag for effective antitumor immune responses.
In the steady state, tumors harbor several populations of dendritic cells (DCs) and myeloid cells that are key regulators of the intratumoral immune environment. Among these cells, migratory CD103 cross-presenting DCs are thought to be critical for tumor-specific CTL responses and tumor resistance. However, it is unclear whether this prominent role also extends to immunotherapy. We used a murine orthotopic mammary tumor model, as well as Clec9A-diphtheria toxin receptor mice that can be depleted of the specialized cross-presenting CD8α and CD103 DC1 subsets, to investigate the role of these DCs in immunotherapy. Treatment with monosodium urate crystals and mycobacteria at the tumor site delayed tumor growth and required DC1s for efficacy. In contrast, treatment with poly I:C was equally effective regardless of DC1 depletion. Neither treatment affected myeloid-derived suppressor cell numbers in the spleen or tumor. Similar experiments using subcutaneous B16 melanoma tumors in BATF3-knockout mice confirmed that CD103 DCs were not necessary for successful poly I:C immunotherapy. Nevertheless, adaptive immune responses were essential for the response to poly I:C, because mice depleted of CD8 T cells or all DC subsets were unable to delay tumor growth. In vivo experiments showed that DC1 and DC2 subsets were able to take up tumor Ags, with DC2s making up the larger proportion of lymph node DCs carrying tumor material. Both DC subsets were able to cross-present OVA to OT-I T cells in vitro. Thus, immunotherapy with poly I:C enables multiple DC subsets to cross-present tumor Ag for effective antitumor immune responses.
Author Kuhn, Sabine
Hyde, Evelyn J
Gilfillan, Connie B
Ronchese, Franca
Yang, Jianping
Baey, Camille
Ruedl, Christiane
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Snippet In the steady state, tumors harbor several populations of dendritic cells (DCs) and myeloid cells that are key regulators of the intratumoral immune...
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StartPage 2978
SubjectTerms Adaptive immunity
Animals
Antitumor activity
CD103 antigen
CD8 antigen
CD8-Positive T-Lymphocytes - immunology
Cell migration
Cross-Priming - immunology
Crystals
Cytotoxicity
Dendritic cells
Dendritic Cells - immunology
Depletion
Diphtheria
Diphtheria toxin
Female
Immune response
Immunotherapy
Immunotherapy - methods
Interferon Inducers - immunology
Lectins, C-Type - immunology
Lymph nodes
Lymphocytes
Lymphocytes T
Mammary gland
Mammary Neoplasms, Experimental - immunology
Melanoma
Melanoma, Experimental - immunology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Myeloid cells
Poly I-C - immunology
Polyinosinic:polycytidylic acid
Receptors, Immunologic - immunology
Rodents
Spleen
T cell receptors
Tumors
Uric acid
Title Clec9A + Dendritic Cells Are Not Essential for Antitumor CD8 + T Cell Responses Induced by Poly I:C Immunotherapy
URI https://www.ncbi.nlm.nih.gov/pubmed/29507107
https://www.proquest.com/docview/2023047581
https://search.proquest.com/docview/2011269460
Volume 200
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