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Article ; Online: Optineurin Guards IFNγ Signaling in Cancer Cells.

Salvagno, Camilla / Cubillos-Ruiz, Juan R

2021 Volume 11, Issue 7, Page(s) 1623–1625

Abstract: In this issue, Du and colleagues uncover that optineurin functions as a key regulator of IFNγ receptor (IFNGR1) stability in malignant cells. Loss of optineurin in colorectal cancer cells causes IFNGR1 degradation, leading to impaired IFNγ signaling, ... ...

Abstract	In this issue, Du and colleagues uncover that optineurin functions as a key regulator of IFNγ receptor (IFNGR1) stability in malignant cells. Loss of optineurin in colorectal cancer cells causes IFNGR1 degradation, leading to impaired IFNγ signaling, decreased MHC-I expression, and enhanced ability to evade adaptive immune control.
MeSH term(s)	Neoplasms/genetics ; Receptors, Interferon
Chemical Substances	Receptors, Interferon
Language	English
Publishing date	2021-07-18
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-21-0362
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Article ; Online: Decoding endoplasmic reticulum stress signals in cancer cells and antitumor immunity.

Salvagno, Camilla / Mandula, Jessica K / Rodriguez, Paulo C / Cubillos-Ruiz, Juan R

Trends in cancer

2022 Volume 8, Issue 11, Page(s) 930–943

Abstract: The tumor microenvironment (TME) provokes endoplasmic reticulum (ER) stress in malignant cells and infiltrating immune populations. Sensing and responding to ER stress is coordinated by the unfolded protein response (UPR), an integrated signaling pathway ...

Abstract	The tumor microenvironment (TME) provokes endoplasmic reticulum (ER) stress in malignant cells and infiltrating immune populations. Sensing and responding to ER stress is coordinated by the unfolded protein response (UPR), an integrated signaling pathway governed by three ER stress sensors: activating transcription factor (ATF6), inositol-requiring enzyme 1α (IRE1α), and protein kinase R (PKR)-like ER kinase (PERK). Persistent UPR activation modulates malignant progression, tumor growth, metastasis, and protective antitumor immunity. Hence, therapies targeting ER stress signaling can be harnessed to elicit direct tumor killing and concomitant anticancer immunity. We highlight recent findings on the role of the ER stress responses in onco-immunology, with an emphasis on genetic vulnerabilities that render tumors highly sensitive to therapeutic UPR modulation.
MeSH term(s)	Humans ; Endoplasmic Reticulum Stress ; Endoribonucleases/metabolism ; Protein Serine-Threonine Kinases ; Neoplasms/pathology ; Inositol ; Tumor Microenvironment
Chemical Substances	Endoribonucleases (EC 3.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Inositol (4L6452S749)
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2022.06.006
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Article: The impact of endoplasmic reticulum stress responses in dendritic cell immunobiology.

Salvagno, Camilla / Cubillos-Ruiz, Juan R

International review of cell and molecular biology

2019 Volume 349, Page(s) 153–176

Abstract: Dendritic cells (DCs) are critical for bridging innate and adaptive immunity. They do so by presenting antigens to T cells, and by expressing diverse molecules that further promote T cell activation, differentiation and memory formation. During this ... ...

Abstract	Dendritic cells (DCs) are critical for bridging innate and adaptive immunity. They do so by presenting antigens to T cells, and by expressing diverse molecules that further promote T cell activation, differentiation and memory formation. During this process, intracellular and extracellular factors can perturb the protein-folding capacity of endoplasmic reticulum (ER) and induce a cellular state of "ER stress," which is controlled and resolved by the unfolded protein response (UPR). Interestingly, various studies have shown that DCs can activate UPR-related pathways even in the absence of global ER stress, and that this process can modulate their normal activity. In other settings, such as cancer, adverse microenvironmental conditions have been demonstrated to evoke severe ER stress and persistent activation of the UPR in tumor-infiltrating DCs. This process disrupts their metabolism and local antigen-presenting capacity, hence impeding the initiation and maintenance of anti-cancer immunity. Here, we review recent findings on how canonical and non-canonical UPR activation impacts DC immunobiology at the steady-state, upon activation via pattern recognition receptors, and under diverse pathological conditions. We also discuss the potential therapeutic implications that targeting the UPR in DCs may have in the context of cancer and in other pathologies such as graft-versus-host disease.
MeSH term(s)	Animals ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Endoplasmic Reticulum Stress/immunology ; Humans ; Unfolded Protein Response
Language	English
Publishing date	2019-09-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2427220-6
ISSN	1937-6448 ; 0074-7696
ISSN	1937-6448 ; 0074-7696
DOI	10.1016/bs.ircmb.2019.08.004
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Article ; Online: Purification of Immune Cell Populations from Freshly Isolated Murine Tumors and Organs by Consecutive Magnetic Cell Sorting and Multi-parameter Flow Cytometry-Based Sorting.

Salvagno, Camilla / de Visser, Karin E

Methods in molecular biology (Clifton, N.J.)

2016 Volume 1458, Page(s) 125–135

Abstract: It is well established that tumors evolve together with nonmalignant cells, such as fibroblasts, endothelial cells, and immune cells. These cells constantly entangle and interact with each other creating the tumor microenvironment. Immune cells can exert ...

Abstract	It is well established that tumors evolve together with nonmalignant cells, such as fibroblasts, endothelial cells, and immune cells. These cells constantly entangle and interact with each other creating the tumor microenvironment. Immune cells can exert both tumor-promoting and tumor-protective functions. Detailed phenotypic and functional characterization of intra-tumoral immune cell subsets has become increasingly important in the field of cancer biology and cancer immunology. In this chapter, we describe a method for isolation of viable and pure immune cell subsets from freshly isolated murine solid tumors and organs. First, we describe a protocol for the generation of single-cell suspensions from tumors and organs using mechanical and enzymatic strategies. In addition, we describe how immune cell subsets can be purified by consecutive magnetic cell sorting and multi-parameter flow cytometry-based cell sorting.
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-3801-8_10
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Article: Exploiting the Immunomodulatory Properties of Chemotherapeutic Drugs to Improve the Success of Cancer Immunotherapy.

Kersten, Kelly / Salvagno, Camilla / de Visser, Karin E

Frontiers in immunology

2015 Volume 6, Page(s) 516

Abstract: Cancer immunotherapy is gaining momentum in the clinic. The current challenge is to understand why a proportion of cancer patients do not respond to cancer immunotherapy, and how this can be translated into the rational design of combinatorial cancer ... ...

Abstract	Cancer immunotherapy is gaining momentum in the clinic. The current challenge is to understand why a proportion of cancer patients do not respond to cancer immunotherapy, and how this can be translated into the rational design of combinatorial cancer immunotherapy strategies aimed at maximizing success of immunotherapy. Here, we discuss how tumors orchestrate an immunosuppressive microenvironment, which contributes to their escape from immune attack. Relieving the immunosuppressive networks in cancer patients is an attractive strategy to extend the clinical success of cancer immunotherapy. Since the clinical availability of drugs specifically targeting immunosuppressive cells or mediators is still limited, an alternative strategy is to use conventional chemotherapy drugs with immunomodulatory properties to improve cancer immunotherapy. We summarize the preclinical and clinical studies that illustrate how the anti-tumor T cell response can be enhanced by chemotherapy-induced relief of immunosuppressive networks. Treatment strategies aimed at combining chemotherapy-induced relief of immunosuppression and T cell-boosting checkpoint inhibitors provide an attractive and clinically feasible approach to overcome intrinsic and acquired resistance to cancer immunotherapy, and to extend the clinical success of cancer immunotherapy.
Language	English
Publishing date	2015-10-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2015.00516
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Article ; Online: hMRP8-ATTAC Mice: A New Model for Conditional and Reversible Neutrophil Ablation.

Duits, Danique E M / Salvagno, Camilla / Raeven, Elisabeth A M / Vrijland, Kim / Stip, Marjolein C / Hau, Cheei-Sing / Kaldenbach, Daphne / de Visser, Karin E

Cells

2022 Volume 11, Issue 15

Abstract: Neutrophils are not only crucial immune cells for the neutralization of pathogens during infections, but they are also key players in tissue repair and cancer. Several methods are available to investigate the in vivo role of neutrophils in these ... ...

Abstract	Neutrophils are not only crucial immune cells for the neutralization of pathogens during infections, but they are also key players in tissue repair and cancer. Several methods are available to investigate the in vivo role of neutrophils in these conditions, including the depletion of neutrophils with neutralizing antibodies against Ly6G, or the blockade of neutrophil recruitment with CXCR2 inhibitors. A limited number of transgenic mouse models were generated that rely on the disruption of genes important for neutrophil development or on the injection of diphtheria toxin to induce neutrophil ablation. However, these methods have various limitations, including a lack of neutrophil specificity, a lack of long-term efficacy, or a lack of the ability to conditionally deplete neutrophils. Therefore, we generated a transgenic mouse model for the inducible and reversible ablation of neutrophils using the ATTAC (Apoptosis Through Targeted Activation of Caspase 8) approach. With the ATTAC strategy, which relies on the expression of the caspase 8-FKBP fusion protein, apoptosis is induced upon administration of a chemical dimerizer (FK506 analogue) that facilitates the dimerization and activation of caspase 8. In order to achieve specific neutrophil depletion, we cloned the ATTAC construct under the human migration inhibitory factor-related protein 8 (hMRP8) promotor. The newly generated hMRP8-ATTAC mice expressed high levels of the transgene in neutrophils, and, as a consequence, dimerizer injection induced an efficient reduction of neutrophil levels in all the organs analyzed under homeostatic conditions. In situations with extensive pressure on the bone marrow to mobilize neutrophils, for instance in the context of cancer, effective neutrophil depletion in this model requires further optimization. In conclusion, we here describe the generation and characterization of a new transgenic model for conditional neutrophil ablation and highlight the need to improve the ATTAC strategy for the depletion of large numbers of rapidly generated short-lived cells, such as neutrophils.
MeSH term(s)	Animals ; Caspase 8/metabolism ; Humans ; Mice ; Mice, Transgenic ; Neoplasms/metabolism ; Neutrophil Infiltration ; Neutrophils/metabolism
Chemical Substances	Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2022-07-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11152346
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Article ; Online: Tumor-associated macrophages promote intratumoral conversion of conventional CD4

Kos, Kevin / Salvagno, Camilla / Wellenstein, Max D / Aslam, Muhammad A / Meijer, Denize A / Hau, Cheei-Sing / Vrijland, Kim / Kaldenbach, Daphne / Raeven, Elisabeth A M / Schmittnaegel, Martina / Ries, Carola H / de Visser, Karin E

Oncoimmunology

2022 Volume 11, Issue 1, Page(s) 2063225

Abstract: While regulatory T cells ( ... ...

Abstract	While regulatory T cells (T
MeSH term(s)	Breast Neoplasms ; Female ; Humans ; Immune Tolerance ; Programmed Cell Death 1 Receptor ; T-Lymphocytes, Regulatory ; Tumor Microenvironment ; Tumor-Associated Macrophages
Chemical Substances	Programmed Cell Death 1 Receptor
Language	English
Publishing date	2022-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.1080/2162402X.2022.2063225
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Article ; Online: Senescence induction dictates response to chemo- and immunotherapy in preclinical models of ovarian cancer.

Paffenholz, Stella V / Salvagno, Camilla / Ho, Yu-Jui / Limjoco, Matthew / Baslan, Timour / Tian, Sha / Kulick, Amanda / de Stanchina, Elisa / Wilkinson, John E / Barriga, Francisco M / Zamarin, Dmitriy / Cubillos-Ruiz, Juan R / Leibold, Josef / Lowe, Scott W

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 5

Abstract: High-grade serous ovarian carcinoma (HGSOC) is a cancer with dismal prognosis due to the limited effectiveness of existing chemo- and immunotherapies. To elucidate mechanisms mediating sensitivity or resistance to these therapies, we developed a fast and ...

Abstract	High-grade serous ovarian carcinoma (HGSOC) is a cancer with dismal prognosis due to the limited effectiveness of existing chemo- and immunotherapies. To elucidate mechanisms mediating sensitivity or resistance to these therapies, we developed a fast and flexible autochthonous mouse model based on somatic introduction of HGSOC-associated genetic alterations into the ovary of immunocompetent mice using tissue electroporation. Tumors arising in these mice recapitulate the metastatic patterns and histological, molecular, and treatment response features of the human disease. By leveraging these models, we show that the ability to undergo senescence underlies the clinically observed increase in sensitivity of homologous recombination (HR)-deficient HGSOC tumors to platinum-based chemotherapy. Further, cGas/STING-mediated activation of a restricted senescence-associated secretory phenotype (SASP) was sufficient to induce immune infiltration and sensitize HR-deficient tumors to immune checkpoint blockade. In sum, our study identifies senescence propensity as a predictor of therapy response and defines a limited SASP profile that appears sufficient to confer added vulnerability to concurrent immunotherapy and, more broadly, provides a blueprint for the implementation of electroporation-based mouse models to reveal mechanisms of oncogenesis and therapy response in HGSOC.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Carcinoma, Ovarian Epithelial/diet therapy ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immunotherapy/methods ; Mice ; Mice, Inbred C57BL ; Ovarian Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2022-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2117754119
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Article ; Online: Inflammatory ER stress responses dictate the immunopathogenic progression of systemic candidiasis.

Awasthi, Deepika / Chopra, Sahil / Cho, Byuri A / Emmanuelli, Alexander / Sandoval, Tito A / Hwang, Sung-Min / Chae, Chang-Suk / Salvagno, Camilla / Tan, Chen / Vasquez-Urbina, Liliana / Fernandez Rodriguez, Jose J / Santagostino, Sara F / Iwawaki, Takao / Romero-Sandoval, E Alfonso / Crespo, Mariano Sanchez / Morales, Diana K / Iliev, Iliyan D / Hohl, Tobias M / Cubillos-Ruiz, Juan R

The Journal of clinical investigation

2023 Volume 133, Issue 17

Abstract: Recognition of pathogen-associated molecular patterns can trigger the inositol-requiring enzyme 1 α (IRE1α) arm of the endoplasmic reticulum (ER) stress response in innate immune cells. This process maintains ER homeostasis and also coordinates diverse ... ...

Abstract	Recognition of pathogen-associated molecular patterns can trigger the inositol-requiring enzyme 1 α (IRE1α) arm of the endoplasmic reticulum (ER) stress response in innate immune cells. This process maintains ER homeostasis and also coordinates diverse immunomodulatory programs during bacterial and viral infections. However, the role of innate IRE1α signaling in response to fungal pathogens remains elusive. Here, we report that systemic infection with the human opportunistic fungal pathogen Candida albicans induced proinflammatory IRE1α hyperactivation in myeloid cells that led to fatal kidney immunopathology. Mechanistically, simultaneous activation of the TLR/IL-1R adaptor protein MyD88 and the C-type lectin receptor dectin-1 by C. albicans induced NADPH oxidase-driven generation of ROS, which caused ER stress and IRE1α-dependent overexpression of key inflammatory mediators such as IL-1β, IL-6, chemokine (C-C motif) ligand 5 (CCL5), prostaglandin E2 (PGE2), and TNF-α. Selective ablation of IRE1α in leukocytes, or treatment with an IRE1α pharmacological inhibitor, mitigated kidney inflammation and prolonged the survival of mice with systemic C. albicans infection. Therefore, controlling IRE1α hyperactivation may be useful for impeding the immunopathogenic progression of disseminated candidiasis.
MeSH term(s)	Humans ; Animals ; Mice ; Protein Serine-Threonine Kinases/metabolism ; Endoribonucleases/metabolism ; Candidiasis ; Endoplasmic Reticulum Stress ; Candida albicans ; Toll-Like Receptors/metabolism ; Adaptor Proteins, Signal Transducing/metabolism
Chemical Substances	Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Toll-Like Receptors ; Adaptor Proteins, Signal Transducing
Language	English
Publishing date	2023-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI167359
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Article ; Online: Tumor-Derived Lysophosphatidic Acid Blunts Protective Type I Interferon Responses in Ovarian Cancer.

Cancer discovery

2022 Volume 12, Issue 8, Page(s) 1904–1921

Abstract: Lysophosphatidic acid (LPA) is a bioactive lipid enriched in the tumor microenvironment of immunosuppressive malignancies such as ovarian cancer. Although LPA enhances the tumorigenic attributes of cancer cells, the immunomodulatory activity of this ... ...

Abstract	Lysophosphatidic acid (LPA) is a bioactive lipid enriched in the tumor microenvironment of immunosuppressive malignancies such as ovarian cancer. Although LPA enhances the tumorigenic attributes of cancer cells, the immunomodulatory activity of this phospholipid messenger remains largely unexplored. Here, we report that LPA operates as a negative regulator of type I interferon (IFN) responses in ovarian cancer. Ablation of the LPA-generating enzyme autotaxin (ATX) in ovarian cancer cells reprogrammed the tumor immune microenvironment, extended host survival, and improved the effects of therapies that elicit protective responses driven by type I IFN. Mechanistically, LPA sensing by dendritic cells triggered PGE2 biosynthesis that suppressed type I IFN signaling via autocrine EP4 engagement. Moreover, we identified an LPA-controlled, immune-derived gene signature associated with poor responses to combined PARP inhibition and PD-1 blockade in patients with ovarian cancer. Controlling LPA production or sensing in tumors may therefore be useful to improve cancer immunotherapies that rely on robust induction of type I IFN. Significance: This study uncovers that ATX-LPA is a central immunosuppressive pathway in the ovarian tumor microenvironment. Ablating this axis sensitizes ovarian cancer hosts to various immunotherapies by unleashing protective type I IFN responses. Understanding the immunoregulatory programs induced by LPA could lead to new biomarkers predicting resistance to immunotherapy in patients with cancer. See related commentary by Conejo-Garcia and Curiel, p. 1841. This article is highlighted in the In This Issue feature, p. 1825.
MeSH term(s)	Female ; Humans ; Interferon Type I ; Lysophospholipids/genetics ; Lysophospholipids/metabolism ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Receptors, Lysophosphatidic Acid/genetics ; Receptors, Lysophosphatidic Acid/metabolism ; Tumor Microenvironment
Chemical Substances	Interferon Type I ; Lysophospholipids ; Receptors, Lysophosphatidic Acid ; lysophosphatidic acid (PG6M3969SG)
Language	English
Publishing date	2022-05-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-21-1181
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