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Species: human
Number of cells: 4371
Number of downloads: 0
Study size: 246MB
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Cancer 
Spatial 
Prostate 

10X Spatial Gene Expression Datasets - Human Prostate Cancer, Adenocarcinoma with Invasive Carcinoma (FFPE)

Spatial Gene Expression Dataset by Space Ranger 1.3.0

5 µm section from Adenocarcinoma of Human Prostate. FFPE tissue purchased from Indivumed Human Tissue Specimens (Indivumed). Block 1E500_Tp12 Section 1 Stage III Total Gleason score: 7 Sex: Male 20x magnification Libraries were prepared following the Visium Spatial Gene Expression Reagent Kits for FFPE User Guide (CG000407 Rev A). Libraries were sequenced on Illumina NovaSeq with approximately 22,964 reads per spot, dual index set SI-TS-F8, 28bp read 1 (16bp Visium spatial barcode, 12bp UMI), 50bp read2 (transcript), 10bp i7 sample barcode and 10bp i5 sample barcode. FASTQ data were analyzed with Space Ranger 1.3. 4371 spots were detected under tissue. Annotated with Adenocarcinoma, Invasive Carcinoma.

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Species: human
Number of cells: 8740
Number of downloads: 1
Study size: 47MB
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White adipose tissue 

Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner (Human - MARS-Seq)

Diego Adhemar Jaitin, Lorenz Adlung, Christoph A Thaiss, Assaf Weiner, Baoguo Li, Helene Descamps, Patrick Lundgren, Camille Bleriot, Zhaoyuan Liu, Aleksandra Deczkowska, Hadas Keren-Shaul, Eyal David, Niv Zmora, Shai Meron Eldar, Nir Lubezky, Oren Shibolet, David A Hill, Mitchell A Lazar, Marco Colonna, Florent Ginhoux, Hagit Shapiro, Eran Elinav, Ido Amit

Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

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Species: human
Number of cells: 3382
Number of downloads: 1
Study size: 26MB
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White adipose tissue 

Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner (Human - 10X)

Diego Adhemar Jaitin, Lorenz Adlung, Christoph A Thaiss, Assaf Weiner, Baoguo Li, Helene Descamps, Patrick Lundgren, Camille Bleriot, Zhaoyuan Liu, Aleksandra Deczkowska, Hadas Keren-Shaul, Eyal David, Niv Zmora, Shai Meron Eldar, Nir Lubezky, Oren Shibolet, David A Hill, Mitchell A Lazar, Marco Colonna, Florent Ginhoux, Hagit Shapiro, Eran Elinav, Ido Amit

Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

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Species: mouse
Number of cells: 10743
Number of downloads: 0
Study size: 97MB
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White adipose tissue 

Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner (Mouse - db/db)

Diego Adhemar Jaitin, Lorenz Adlung, Christoph A Thaiss, Assaf Weiner, Baoguo Li, Helene Descamps, Patrick Lundgren, Camille Bleriot, Zhaoyuan Liu, Aleksandra Deczkowska, Hadas Keren-Shaul, Eyal David, Niv Zmora, Shai Meron Eldar, Nir Lubezky, Oren Shibolet, David A Hill, Mitchell A Lazar, Marco Colonna, Florent Ginhoux, Hagit Shapiro, Eran Elinav, Ido Amit

Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

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Species: mouse
Number of cells: 9882
Number of downloads: 0
Study size: 100MB
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White adipose tissue 

Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner (Mouse - Trem2 KO)

Diego Adhemar Jaitin, Lorenz Adlung, Christoph A Thaiss, Assaf Weiner, Baoguo Li, Helene Descamps, Patrick Lundgren, Camille Bleriot, Zhaoyuan Liu, Aleksandra Deczkowska, Hadas Keren-Shaul, Eyal David, Niv Zmora, Shai Meron Eldar, Nir Lubezky, Oren Shibolet, David A Hill, Mitchell A Lazar, Marco Colonna, Florent Ginhoux, Hagit Shapiro, Eran Elinav, Ido Amit

Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

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Species: mouse
Number of cells: 20593
Number of downloads: 0
Study size: 204MB
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White adipose tissue 

Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner (Mouse - Wild-type)

Diego Adhemar Jaitin, Lorenz Adlung, Christoph A Thaiss, Assaf Weiner, Baoguo Li, Helene Descamps, Patrick Lundgren, Camille Bleriot, Zhaoyuan Liu, Aleksandra Deczkowska, Hadas Keren-Shaul, Eyal David, Niv Zmora, Shai Meron Eldar, Nir Lubezky, Oren Shibolet, David A Hill, Mitchell A Lazar, Marco Colonna, Florent Ginhoux, Hagit Shapiro, Eran Elinav, Ido Amit

Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

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Species: human
Number of cells: 29984
Number of downloads: 1
Study size: 1GB
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Cancer 
Brain 
Glioblastoma 

Single-cell RNA-seq reveals that glioblastoma recapitulates a normal neurodevelopmental hierarchy (Enriched glioblastoma stem cells)

Charles P. Couturier, Shamini Ayyadhury, Phuong U. Le, Javad Nadaf, Jean Monlong, Gabriele Riva, Redouane Allache, Salma Baig, Xiaohua Yan, Mathieu Bourgey, Changseok Lee, Yu Chang David Wang, V. Wee Yong, Marie-Christine Guiot, Hamed Najafabadi, Bratislav Misic, Jack Antel, Guillaume Bourque, Jiannis Ragoussis, Kevin Petrecca

Cancer stem cells are critical for cancer initiation, development, and treatment resistance. Our understanding of these processes, and how they relate to glioblastoma heterogeneity, is limited. To overcome these limitations, we performed single-cell RNA sequencing on 53586 adult glioblastoma cells and 22637 normal human fetal brain cells, and compared the lineage hierarchy of the developing human brain to the transcriptome of cancer cells. We find a conserved neural tri-lineage cancer hierarchy centered around glial progenitor-like cells. We also find that this progenitor population contains the majority of the cancer’s cycling cells, and, using RNA velocity, is often the originator of the other cell types. Finally, we show that this hierarchal map can be used to identify therapeutic targets specific to progenitor cancer stem cells. Our analyses show that normal brain development reconciles glioblastoma development, suggests a possible origin for glioblastoma hierarchy, and helps to identify cancer stem cell-specific targets.

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Species: human
Number of cells: 44050
Number of downloads: 2
Study size: 1GB
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Cancer 
Brain 
Glioblastoma 

Single-cell RNA-seq reveals that glioblastoma recapitulates a normal neurodevelopmental hierarchy (scRNA-seq - Whole tumor)

Charles P. Couturier, Shamini Ayyadhury, Phuong U. Le, Javad Nadaf, Jean Monlong, Gabriele Riva, Redouane Allache, Salma Baig, Xiaohua Yan, Mathieu Bourgey, Changseok Lee, Yu Chang David Wang, V. Wee Yong, Marie-Christine Guiot, Hamed Najafabadi, Bratislav Misic, Jack Antel, Guillaume Bourque, Jiannis Ragoussis, Kevin Petrecca

Cancer stem cells are critical for cancer initiation, development, and treatment resistance. Our understanding of these processes, and how they relate to glioblastoma heterogeneity, is limited. To overcome these limitations, we performed single-cell RNA sequencing on 53586 adult glioblastoma cells and 22637 normal human fetal brain cells, and compared the lineage hierarchy of the developing human brain to the transcriptome of cancer cells. We find a conserved neural tri-lineage cancer hierarchy centered around glial progenitor-like cells. We also find that this progenitor population contains the majority of the cancer’s cycling cells, and, using RNA velocity, is often the originator of the other cell types. Finally, we show that this hierarchal map can be used to identify therapeutic targets specific to progenitor cancer stem cells. Our analyses show that normal brain development reconciles glioblastoma development, suggests a possible origin for glioblastoma hierarchy, and helps to identify cancer stem cell-specific targets.

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Species: human
Number of cells: 37156
Number of downloads: 10
Study size: 445MB
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Crohn disease 
Ileum 
lamina propria 

Single-cell analyses of Crohn's disease tissues reveal intestinal intraepithelial T cells heterogeneity and altered subset distributions (Lamina propria)

Natalia Jaeger, Ramya Gamini, Marina Cella, Jorge L. Schettini, Mattia Bugatti, Shanrong Zhao, Charles V. Rosadini, Ekaterina Esaulova, Blanda Di Luccia, Baylee Kinnett, William Vermi, Maxim N. Artyomov, Thomas A. Wynn, Ramnik J. Xavier, Scott A. Jelinsky, Marco Colonna

Crohn’s disease (CD) is a chronic transmural inflammation of intestinal segments caused by dysregulated interaction between microbiome and gut immune system. Here, we profile, via multiple single-cell technologies, T cells purified from the intestinal epithelium and lamina propria (LP) from terminal ileum resections of adult severe CD cases. We find that intraepithelial lymphocytes (IEL) contain several unique T cell subsets, including NKp30+γδT cells expressing RORγt and producing IL-26 upon NKp30 engagement. Further analyses comparing tissues from non-inflamed and inflamed regions of patients with CD versus healthy controls show increased activated TH17 but decreased CD8+T, γδT, TFH and Treg cells in inflamed tissues. Similar analyses of LP find increased CD8+, as well as reduced CD4+T cells with an elevated TH17 over Treg/TFH ratio. Our analyses of CD tissues thus suggest a potential link, pending additional validations, between transmural inflammation, reduced IEL γδT cells and altered spatial distribution of IEL and LP T cell subsets.

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Species: human
Number of cells: 21052
Number of downloads: 12
Study size: 281MB
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Crohn disease 

Single-cell analyses of Crohn's disease tissues reveal intestin-al intraepithelial T cells heterogeneity and altered subset distributions (Intraepithelial lymphocyte)

Natalia Jaeger, Ramya Gamini, Marina Cella, Jorge L. Schettini, Mattia Bugatti, Shanrong Zhao, Charles V. Rosadini, Ekaterina Esaulova, Blanda Di Luccia, Baylee Kinnett, William Vermi, Maxim N. Artyomov, Thomas A. Wynn, Ramnik J. Xavier, Scott A. Jelinsky, Marco Colonna

Crohn's disease (CD) is a chronic transmural inflammation of intestinal segments caused by dysregulated interaction between microbiome and gut immune system. Here, we profile, via multiple single-cell technologies, T cells purified from the intestinal epithelium and lamina propria (LP) from terminal ileum resections of adult severe CD cases. We find that intraepithelial lymphocytes (IEL) contain several unique T cell subsets, including NKp30+<ce><b3><ce><b4>T cells expressing ROR<ce><b3>t and producing IL-26 upon NKp30 engagement. Further analyses comparing tissues from non-inflamed and inflamed regions of patients with CD versus healthy controls show increased activated TH17 but decreased CD8+T, <ce><b3><ce><b4>T, TFH and Treg cells in inflamed tissues. Similar analyses of LP find increased CD8+, as well as reduced CD4+T cells with an elevated TH17 over Treg/TFH ratio. Our analyses of CD tissues thus suggest a potential link, pending additional validations, between transmural inflammation, reduced IEL <ce><b3><ce><b4>T cells and altered spatial distribution of IEL and LP T cell subsets.

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Species: mouse
Number of cells: 39298
Number of downloads: 9
Study size: 665MB
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Heart 
JQ1 treatment 

A transcriptional switch governs fibroblast activation in heart disease (scRNA-seq)

Michael Alexanian, Pawel F. Przytycki, Rudi Micheletti, Arun Padmanabhan, Lin Ye, Joshua G. Travers, Barbara Gonzalez-Teran, Ana Catarina Silva, Qiming Duan, Sanjeev S. Ranade, Franco Felix, Ricardo Linares-Saldana, Li Li, Clara Youngna Lee, Nandhini Sadagopan, Angelo Pelonero, Yu Huang, Gaia Andreoletti, Rajan Jain, Timothy A. McKinsey, Michael G. Rosenfeld, Casey A. Gifford, Katherine S. Pollard, Saptarsi M. Haldar, Deepak Srivastava

In diseased organs, stress-activated signalling cascades alter chromatin, thereby triggering maladaptive cell state transitions. Fibroblast activation is a common stress response in tissues that worsens lung, liver, kidney and heart disease, yet its mechanistic basis remains unclear. Pharmacological inhibition of bromodomain and extra-terminal domain (BET) proteins alleviates cardiac dysfunction, providing a tool to interrogate and modulate cardiac cell states as a potential therapeutic approach. Here we use single-cell epigenomic analyses of hearts dynamically exposed to BET inhibitors to reveal a reversible transcriptional switch that underlies the activation of fibroblasts. Resident cardiac fibroblasts demonstrated robust toggling between the quiescent and activated state in a manner directly correlating with BET inhibitor exposure and cardiac function. Single-cell chromatin accessibility revealed previously undescribed DNA elements, the accessibility of which dynamically correlated with cardiac performance. Among the most dynamic elements was an enhancer that regulated the transcription factor MEOX1, which was specifically expressed in activated fibroblasts, occupied putative regulatory elements of a broad fibrotic gene program and was required for TGFβ-induced fibroblast activation. Selective CRISPR inhibition of the single most dynamic cis-element within the enhancer blocked TGFβ-induced Meox1 activation. We identify MEOX1 as a central regulator of fibroblast activation associated with cardiac dysfunction and demonstrate its upregulation after activation of human lung, liver and kidney fibroblasts. The plasticity and specificity of BET-dependent regulation of MEOX1 in tissue fibroblasts provide previously unknown trans- and cis-targets for treating fibrotic disease.

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Species: human
Number of cells: 93218
Number of downloads: 11
Study size: 2GB
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Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (All)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 16872
Number of downloads: 11
Study size: 200MB
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Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (T and NK)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 9885
Number of downloads: 5
Study size: 300MB
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Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (Fibroblast)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 13123
Number of downloads: 4
Study size: 254MB
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Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (Myeloid)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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