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Species: human
Number of cells: 58145
Number of downloads: 2
Study size: 2GB
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Cortex 
Brain development 
Neuroepithelial cell 

Single-cell atlas of early human brain development highlights heterogeneity of human neuroepithelial cells and early radial glia (Cortex)

Ugomma C. Eze, Aparna Bhaduri, Maximilian Haeussler, Tomasz J. Nowakowski, Arnold R. Kriegstein

The human cortex comprises diverse cell types that emerge from an initially uniform neuroepithelium that gives rise to radial glia, the neural stem cells of the cortex. To characterize the earliest stages of human brain development, we performed single-cell RNA-sequencing across regions of the developing human brain, including the telencephalon, diencephalon, midbrain, hindbrain and cerebellum. We identify nine progenitor populations physically proximal to the telencephalon, suggesting more heterogeneity than previously described, including a highly prevalent mesenchymal-like population that disappears once neurogenesis begins. Comparison of human and mouse progenitor populations at corresponding stages identifies two progenitor clusters that are enriched in the early stages of human cortical development. We also find that organoid systems display low fidelity to neuroepithelial and early radial glia cell types, but improve as neurogenesis progresses. Overall, we provide a comprehensive molecular and spatial atlas of early stages of human brain and cortical development.

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Species: mouse
Number of cells: 44130
Number of downloads: 6
Study size: 1GB
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Immunology 
Skin 
Inflammation 
Oxazolone 
Imiquimod 

Single-Cell Profiling Reveals Divergent, Globally Patterned Immune Responses in Murine Skin Inflammation (RNA - ADT - Immune - Figure 1)

Yale Liu, Christopher Cook, Andrew J Sedgewick, Shuyi Zhang, Marlys S Fassett, Roberto R Ricardo-Gonzalez, Paymann Harirchian, Sakeen W Kashem, Sho Hanakawa, Jacob R Leistico, Jeffrey P North, Mark A Taylor, Wei Zhang, Mao-Qiang Man, Alexandra Charruyer, Nadejda Beliakova-Bethell, Stephen C Benz, Ruby Ghadially, Theodora M Mauro, Daniel H Kaplan, Kenji Kabashima, Jaehyuk Choi, Jun S Song, Raymond J Cho, Jeffrey B Cheng

Inflammatory response heterogeneity has impeded high-resolution dissection of diverse immune cell populations during activation. We characterize mouse cutaneous immune cells by single-cell RNA sequencing, after inducing inflammation using imiquimod and oxazolone dermatitis models. We identify 13 CD45+ subpopulations, which broadly represent most functionally characterized immune cell types. Oxazolone pervasively upregulates Jak2/Stat3 expression across T cells and antigen-presenting cells (APCs). Oxazolone also induces Il4/Il13 expression in newly infiltrating basophils, and Il4ra and Ccl24, most prominently in APCs. In contrast, imiquimod broadly upregulates Il17/Il22 and Ccl4/Ccl5. A comparative analysis of single-cell inflammatory transcriptional responses reveals that APC response to oxazolone is tightly restricted by cell identity, whereas imiquimod enforces shared programs on multiple APC populations in parallel. These global molecular patterns not only contrast immune responses on a systems level but also suggest that the mechanisms of new sources of inflammation can eventually be deduced by comparison to known signatures.

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Species: mouse
Number of cells: 52086
Number of downloads: 4
Study size: 1GB
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Immunology 
Skin 
Inflammation 
Oxazolone 
Imiquimod 

Single-Cell Profiling Reveals Divergent, Globally Patterned Immune Responses in Murine Skin Inflammation (RNA - ADT - Integrated - Figure S1)

Yale Liu, Christopher Cook, Andrew J Sedgewick, Shuyi Zhang, Marlys S Fassett, Roberto R Ricardo-Gonzalez, Paymann Harirchian, Sakeen W Kashem, Sho Hanakawa, Jacob R Leistico, Jeffrey P North, Mark A Taylor, Wei Zhang, Mao-Qiang Man, Alexandra Charruyer, Nadejda Beliakova-Bethell, Stephen C Benz, Ruby Ghadially, Theodora M Mauro, Daniel H Kaplan, Kenji Kabashima, Jaehyuk Choi, Jun S Song, Raymond J Cho, Jeffrey B Cheng

Inflammatory response heterogeneity has impeded high-resolution dissection of diverse immune cell populations during activation. We characterize mouse cutaneous immune cells by single-cell RNA sequencing, after inducing inflammation using imiquimod and oxazolone dermatitis models. We identify 13 CD45+ subpopulations, which broadly represent most functionally characterized immune cell types. Oxazolone pervasively upregulates Jak2/Stat3 expression across T cells and antigen-presenting cells (APCs). Oxazolone also induces Il4/Il13 expression in newly infiltrating basophils, and Il4ra and Ccl24, most prominently in APCs. In contrast, imiquimod broadly upregulates Il17/Il22 and Ccl4/Ccl5. A comparative analysis of single-cell inflammatory transcriptional responses reveals that APC response to oxazolone is tightly restricted by cell identity, whereas imiquimod enforces shared programs on multiple APC populations in parallel. These global molecular patterns not only contrast immune responses on a systems level but also suggest that the mechanisms of new sources of inflammation can eventually be deduced by comparison to known signatures.

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Species: human
Number of cells: 4064
Number of downloads: 8
Study size: 93MB
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Immunology 
Immunotherapy 
Mutation 
Rituximab 
Primary immune thrombocytopenia 
Autoimmune 

Rituximab-resistant splenic memory B cells and newly engaged naive B cells fuel relapses in patients with immune thrombocytopenia (Final Transcript Counts)

Etienne Crickx, Pascal Chappert, Aurélien Sokal, Sandra Weller, Imane Azzaoui, Alexis Vandenberghe, Guillaume Bonnard, Geoffrey Rossi, Tatiana Fadeev, Sébastien Storck, Jehane Fadlallah, Véronique Meignin, Etienne Rivière, Sylvain Audia, Bertrand Godeau, Marc Michel, Jean-Claude Weill, Claude-Agnès Reynaud, Matthieu Mahévas

Rituximab (RTX), an antibody targeting CD20, is widely used as a first-line therapeutic strategy in B cell–mediated autoimmune diseases. However, a large proportion of patients either do not respond to the treatment or relapse during B cell reconstitution. Here, we characterize the cellular basis responsible for disease relapse in secondary lymphoid organs in humans, taking advantage of the opportunity offered by therapeutic splenectomy in patients with relapsing immune thrombocytopenia. By analyzing the B and plasma cell immunoglobulin gene repertoire at bulk and antigen-specific single-cell level, we demonstrate that relapses are associated with two responses coexisting in germinal centers and involving preexisting mutated memory B cells that survived RTX treatment and naive B cells generated upon reconstitution of the B cell compartment. To identify distinctive characteristics of the memory B cells that escaped RTX-mediated depletion, we analyzed RTX refractory patients who did not respond to treatment at the time of B cell depletion. We identified, by single-cell RNA sequencing (scRNA-seq) analysis, a population of quiescent splenic memory B cells that present a unique, yet reversible, RTX-shaped phenotype characterized by down-modulation of B cell–specific factors and expression of prosurvival genes. Our results clearly demonstrate that these RTX-resistant autoreactive memory B cells reactivate as RTX is cleared and give rise to plasma cells and further germinal center reactions. Their continued surface expression of CD19 makes them efficient targets for current anti-CD19 therapies. This study thus identifies a pathogenic contributor to autoimmune diseases that can be targeted by available therapeutic agents.

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Species: human
Number of cells: 4064
Number of downloads: 3
Study size: 88MB
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Immunology 
Immunotherapy 
Mutation 
Rituximab 
Primary immune thrombocytopenia 
Autoimmune 

Rituximab-resistant splenic memory B cells and newly engaged naive B cells fuel relapses in patients with immune thrombocytopenia (Barcode Counts - post UMI correction)

Etienne Crickx, Pascal Chappert, Aurélien Sokal, Sandra Weller, Imane Azzaoui, Alexis Vandenberghe, Guillaume Bonnard, Geoffrey Rossi, Tatiana Fadeev, Sébastien Storck, Jehane Fadlallah, Véronique Meignin, Etienne Rivière, Sylvain Audia, Bertrand Godeau, Marc Michel, Jean-Claude Weill, Claude-Agnès Reynaud, Matthieu Mahévas

Rituximab (RTX), an antibody targeting CD20, is widely used as a first-line therapeutic strategy in B cell–mediated autoimmune diseases. However, a large proportion of patients either do not respond to the treatment or relapse during B cell reconstitution. Here, we characterize the cellular basis responsible for disease relapse in secondary lymphoid organs in humans, taking advantage of the opportunity offered by therapeutic splenectomy in patients with relapsing immune thrombocytopenia. By analyzing the B and plasma cell immunoglobulin gene repertoire at bulk and antigen-specific single-cell level, we demonstrate that relapses are associated with two responses coexisting in germinal centers and involving preexisting mutated memory B cells that survived RTX treatment and naive B cells generated upon reconstitution of the B cell compartment. To identify distinctive characteristics of the memory B cells that escaped RTX-mediated depletion, we analyzed RTX refractory patients who did not respond to treatment at the time of B cell depletion. We identified, by single-cell RNA sequencing (scRNA-seq) analysis, a population of quiescent splenic memory B cells that present a unique, yet reversible, RTX-shaped phenotype characterized by down-modulation of B cell–specific factors and expression of prosurvival genes. Our results clearly demonstrate that these RTX-resistant autoreactive memory B cells reactivate as RTX is cleared and give rise to plasma cells and further germinal center reactions. Their continued surface expression of CD19 makes them efficient targets for current anti-CD19 therapies. This study thus identifies a pathogenic contributor to autoimmune diseases that can be targeted by available therapeutic agents.

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Species: human
Number of cells: 4064
Number of downloads: 3
Study size: 110MB
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Immunology 
Immunotherapy 
Mutation 
Rituximab 
Primary immune thrombocytopenia 
Autoimmune 

Rituximab-resistant splenic memory B cells and newly engaged naive B cells fuel relapses in patients with immune thrombocytopenia (Read Counts - prior to UMI correction)

Etienne Crickx, Pascal Chappert, Aurélien Sokal, Sandra Weller, Imane Azzaoui, Alexis Vandenberghe, Guillaume Bonnard, Geoffrey Rossi, Tatiana Fadeev, Sébastien Storck, Jehane Fadlallah, Véronique Meignin, Etienne Rivière, Sylvain Audia, Bertrand Godeau, Marc Michel, Jean-Claude Weill, Claude-Agnès Reynaud, Matthieu Mahévas

Rituximab (RTX), an antibody targeting CD20, is widely used as a first-line therapeutic strategy in B cell–mediated autoimmune diseases. However, a large proportion of patients either do not respond to the treatment or relapse during B cell reconstitution. Here, we characterize the cellular basis responsible for disease relapse in secondary lymphoid organs in humans, taking advantage of the opportunity offered by therapeutic splenectomy in patients with relapsing immune thrombocytopenia. By analyzing the B and plasma cell immunoglobulin gene repertoire at bulk and antigen-specific single-cell level, we demonstrate that relapses are associated with two responses coexisting in germinal centers and involving preexisting mutated memory B cells that survived RTX treatment and naive B cells generated upon reconstitution of the B cell compartment. To identify distinctive characteristics of the memory B cells that escaped RTX-mediated depletion, we analyzed RTX refractory patients who did not respond to treatment at the time of B cell depletion. We identified, by single-cell RNA sequencing (scRNA-seq) analysis, a population of quiescent splenic memory B cells that present a unique, yet reversible, RTX-shaped phenotype characterized by down-modulation of B cell–specific factors and expression of prosurvival genes. Our results clearly demonstrate that these RTX-resistant autoreactive memory B cells reactivate as RTX is cleared and give rise to plasma cells and further germinal center reactions. Their continued surface expression of CD19 makes them efficient targets for current anti-CD19 therapies. This study thus identifies a pathogenic contributor to autoimmune diseases that can be targeted by available therapeutic agents.

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Species: human
Number of cells: 38274
Number of downloads: 26
Study size: 954MB
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Skin 
Inflammation 
Seq-Well S3 

Second-Strand Synthesis-Based Massively Parallel scRNA-Seq Reveals Cellular States and Molecular Features of Human Inflammatory Skin Pathologies

Travis K.Hughes, Marc H.Wadsworth II, Todd M.Gierahn, Tran Do, David Weiss, Priscila R.Andrade, Feiyang Ma, Bruno J.de Andrade Silva, Shuai Shao, Lam C.Tsoi, Jose Ordovas-Montanes, Johann E.Gudjonsson, Robert L.Modlin, J. Christopher Love, Alex K.Shalek

High-throughput single-cell RNA-sequencing (scRNA-seq) methodologies enable characterization of complex biological samples by increasing the number of cells that can be profiled contemporaneously. Nevertheless, these approaches recover less information per cell than low-throughput strategies. To accurately report the expression of key phenotypic features of cells, scRNA-seq platforms are needed that are both high fidelity and high throughput. To address this need, we created Seq-Well S3 (<e2><80><98><e2><80><98>Second-Strand Synthesis<e2><80><99><e2><80><99>), a massively parallel scRNA-seq protocol that uses a randomly primed second-strand synthesis to recover complementary DNA (cDNA) molecules that were successfully reverse transcribed but to which a second oligonucleotide handle, necessary for subsequent whole transcriptome amplification, was not appended due to inefficient template switching. Seq-Well S3 increased the efficiency of transcript capture and gene detection compared with that of previous iterations by up to 10- and 5-fold, respectively. We used SeqWell S3 to chart the transcriptional landscape of five human inflammatory skin diseases, thus providing a resource for the further study of human skin inflammation.

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Species: mouse
Number of cells: 7665
Number of downloads: 14
Study size: 156MB
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Efferocytosis 
Macrophages 
Peritoneum 

Single-cell RNA sequencing uncovers heterogenous transcriptional signatures in macrophages during efferocytosis

Connor Lantz, Behram Radmanesh, Esther Liu, Edward B. Thorp, Jennie Lin

Efferocytosis triggers cellular reprogramming, including the induction of mRNA transcripts which encode anti-inflammatory cytokines that promote inflammation resolution. Our current understanding of this transcriptional response is largely informed from analysis of bulk phagocyte populations; however, this precludes the resolution of heterogeneity between individual macrophages and macrophage subsets. Moreover, phagocytes may contain so called "passenger" transcripts that originate from engulfed apoptotic bodies, thus obscuring the true transcriptional reprogramming of the phagocyte. To define the transcriptional diversity during efferocytosis, we utilized single-cell mRNA sequencing after co-cultivating macrophages with apoptotic cells. Importantly, transcriptomic analyses were performed after validating the disappearance of apoptotic cell-derived RNA sequences. Our findings reveal new heterogeneity of the efferocytic response at a single-cell resolution, particularly evident between F4/80+ MHCIILO and F4/80- MHCIIHI macrophage sub-populations. After exposure to apoptotic cells, the F4/80+ MHCIILO subset significantly induced pathways associated with tissue and cellular homeostasis, while the F4/80- MHCIIHI subset downregulated these putative signaling axes. Ablation of a canonical efferocytosis receptor, MerTK, blunted efferocytic signatures and led to the escalation of cell death-associated transcriptional signatures in F4/80+ MHCIILO macrophages. Taken together, our results newly elucidate the heterogenous transcriptional response of single-cell peritoneal macrophages after exposure to apoptotic cells.

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Species: human
Number of cells: 1089
Number of downloads: 6
Study size: 163MB
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Immunology 
Esophagus 
Eosinophilic esophagitis 

Single-cell RNA sequencing identifies inflammatory tissue T cells in eosinophilic esophagitis (Gencode v26)

Ting Wen, Bruce J. Aronow, Yrina Rochman, Mark Rochman, Kiran KC, Phil J. Dexheimer, Philip Putnam, Vincent Mukkada, Heather Foote, Kira Rehn, Sam Darko, Daniel Douek, Marc E. Rothenberg

T cell heterogeneity is highly relevant to allergic disorders. We resolved the heterogeneity of human tissue CD3+ T cells during allergic inflammation, focusing on a tissue-specific allergic disease, eosinophilic esophagitis (EoE). We investigated 1088 single T cells derived from patients with a spectrum of disease activity. Eight disparate tissue T cell subtypes (designated T1–T8) were identified, with T7 and T8 enriched in the diseased tissue. The phenotypes of T7 and T8 resemble putative Treg (FOXP3+) and effector Th2-like (GATA3+) cells, respectively. Prodigious levels of IL-5 and IL-13 were confined to HPGDS+ CRTH2+IL-17RB+FFAR3+CD4+ T8 effector Th2 cells. EoE severity closely paralleled a lipid/fatty acid–induced activation node highlighted by the expression of the short-chain fatty acid receptor FFAR3. Ligands for FFAR3 induced Th2 cytokine production from human and murine T cells, including in an in vivo allergy model. Therefore, we elucidated the defining characteristics of tissue-residing CD3+ T cells in EoE, a specific enrichment of CD4+ Treg and effector Th2 cells, confinement of type 2 cytokine production to the CD4+ effector population, a highly likely role for FFAR3 in amplifying local Th2 responses in EoE, and a resource to further dissect tissue lymphocytes and allergic responses.

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Species: human
Number of cells: 1089
Number of downloads: 3
Study size: 135MB
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Immunology 
Esophagus 
Eosinophilic esophagitis 

Single-cell RNA sequencing identifies inflammatory tissue T cells in eosinophilic esophagitis (UCSC)

Ting Wen, Bruce J. Aronow, Yrina Rochman, Mark Rochman, Kiran KC, Phil J. Dexheimer, Philip Putnam, Vincent Mukkada, Heather Foote, Kira Rehn, Sam Darko, Daniel Douek, Marc E. Rothenberg

T cell heterogeneity is highly relevant to allergic disorders. We resolved the heterogeneity of human tissue CD3+ T cells during allergic inflammation, focusing on a tissue-specific allergic disease, eosinophilic esophagitis (EoE). We investigated 1088 single T cells derived from patients with a spectrum of disease activity. Eight disparate tissue T cell subtypes (designated T1–T8) were identified, with T7 and T8 enriched in the diseased tissue. The phenotypes of T7 and T8 resemble putative Treg (FOXP3+) and effector Th2-like (GATA3+) cells, respectively. Prodigious levels of IL-5 and IL-13 were confined to HPGDS+ CRTH2+IL-17RB+FFAR3+CD4+ T8 effector Th2 cells. EoE severity closely paralleled a lipid/fatty acid–induced activation node highlighted by the expression of the short-chain fatty acid receptor FFAR3. Ligands for FFAR3 induced Th2 cytokine production from human and murine T cells, including in an in vivo allergy model. Therefore, we elucidated the defining characteristics of tissue-residing CD3+ T cells in EoE, a specific enrichment of CD4+ Treg and effector Th2 cells, confinement of type 2 cytokine production to the CD4+ effector population, a highly likely role for FFAR3 in amplifying local Th2 responses in EoE, and a resource to further dissect tissue lymphocytes and allergic responses.

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Species: human
Number of cells: 11190
Number of downloads: 8
Study size: 121MB
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Immunology 
immuno-oncology 
Immuno-suppressive 
Blood 
Non-small-cell lung cancer 
Trajectory analysis 
MDSC 

Analysis of classical neutrophils and polymorphonuclear myeloid-derived suppressor cells in cancer patients and tumor-bearing mice (Human)

Filippo Veglia, Ayumi Hashimoto, Harsh Dweep, Emilio Sanseviero, Alessandra De Leo, Evgenii Tcyganov, Andrew Kossenkov, Charles Mulligan, Brian Nam, Gregory Masters, Jaymala Patel, Vipul Bhargava, Patrick Wilkinson, Denis Smirnov, Manuel A Sepulveda, Sunil Singhal, Evgeniy B Eruslanov, Razvan Cristescu, Andrey Loboda, Yulia Nefedova, Dmitry I Gabrilovich

In this study, using single-cell RNA-seq, cell mass spectrometry, flow cytometry, and functional analysis, we characterized the heterogeneity of polymorphonuclear neutrophils (PMNs) in cancer. We describe three populations of PMNs in tumor-bearing mice: classical PMNs, polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs), and activated PMN-MDSCs with potent immune suppressive activity. In spleens of mice, PMN-MDSCs gradually replaced PMNs during tumor progression. Activated PMN-MDSCs were found only in tumors, where they were present at the very early stages of the disease. These populations of PMNs in mice could be separated based on the expression of CD14. In peripheral blood of cancer patients, we identified two distinct populations of PMNs with characteristics of classical PMNs and PMN-MDSCs. The gene signature of tumor PMN-MDSCs was similar to that in mouse activated PMN-MDSCs and was closely associated with negative clinical outcome in cancer patients. Thus, we provide evidence that PMN-MDSCs are a distinct population of PMNs with unique features and potential for selective targeting opportunities.

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Species: mouse
Number of cells: 66854
Number of downloads: 5
Study size: 796MB
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Immunology 
Immuno-suppressive 
MDSC 
Immuno-oncology 
Spleen 

Analysis of classical neutrophils and polymorphonuclear myeloid-derived suppressor cells in cancer patients and tumor-bearing mice (Mouse)

Filippo Veglia, Ayumi Hashimoto, Harsh Dweep, Emilio Sanseviero, Alessandra De Leo, Evgenii Tcyganov, Andrew Kossenkov, Charles Mulligan, Brian Nam, Gregory Masters, Jaymala Patel, Vipul Bhargava, Patrick Wilkinson, Denis Smirnov, Manuel A Sepulveda, Sunil Singhal, Evgeniy B Eruslanov, Razvan Cristescu, Andrey Loboda, Yulia Nefedova, Dmitry I Gabrilovich

In this study, using single-cell RNA-seq, cell mass spectrometry, flow cytometry, and functional analysis, we characterized the heterogeneity of polymorphonuclear neutrophils (PMNs) in cancer. We describe three populations of PMNs in tumor-bearing mice: classical PMNs, polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs), and activated PMN-MDSCs with potent immune suppressive activity. In spleens of mice, PMN-MDSCs gradually replaced PMNs during tumor progression. Activated PMN-MDSCs were found only in tumors, where they were present at the very early stages of the disease. These populations of PMNs in mice could be separated based on the expression of CD14. In peripheral blood of cancer patients, we identified two distinct populations of PMNs with characteristics of classical PMNs and PMN-MDSCs. The gene signature of tumor PMN-MDSCs was similar to that in mouse activated PMN-MDSCs and was closely associated with negative clinical outcome in cancer patients. Thus, we provide evidence that PMN-MDSCs are a distinct population of PMNs with unique features and potential for selective targeting opportunities.

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Species: human
Number of cells: 89887
Number of downloads: 95
Study size: 2GB
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Immunology 
Immuno-suppressive 
Lung 
Non-small-cell lung cancer 
Trajectory analysis 
Lung cancer 
Mutation 
MDSC 
Immuno-oncology 

Single-cell profiling of tumor heterogeneity and the microenvironment in advanced non-small cell lung cancer

Fengying Wu, Jue Fan, Yayi He, Anwen Xiong, Jia Yu, Yixin Li, Yan Zhang, Wencheng Zhao, Fei Zhou, Wei Li, Jie Zhang, Xiaosheng Zhang, Meng Qiao, Guanghui Gao, Shanhao Chen, Xiaoxia Chen, Xuefei Li, Likun Hou, Chunyan Wu, Chunxia Su, Shengxiang Ren, Margarete Odenthal, Reinhard Buettner, Nan Fang, Caicun Zhou

Lung cancer is a highly heterogeneous disease. Cancer cells and cells within the tumor microenvironment together determine disease progression, as well as response to or escape from treatment. To map the cell type-specific transcriptome landscape of cancer cells and their tumor microenvironment in advanced non-small cell lung cancer (NSCLC), we analyze 42 tissue biopsy samples from stage III/IV NSCLC patients by single cell RNA sequencing and present the large scale, single cell resolution profiles of advanced NSCLCs. In addition to cell types described in previous single cell studies of early stage lung cancer, we are able to identify rare cell types in tumors such as follicular dendritic cells and T helper 17 cells. Tumors from different patients display large heterogeneity in cellular composition, chromosomal structure, developmental trajectory, intercellular signaling network and phenotype dominance. Our study also reveals a correlation of tumor heterogeneity with tumor associated neutrophils, which might help to shed light on their function in NSCLC.

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Species: human
Number of cells: 97631
Number of downloads: 11
Study size: 3GB
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Immunology 
immuno-oncology 
tumor microenvironment 
Immuno-suppressive 
Cancer-associated fibroblast 
Esophageal cancer 
Esophageal squamous-cell carcinoma 
Esophagus 

Dissecting esophageal squamous-cell carcinoma ecosystem by single-cell transcriptomic analysis (CD45 negative)

Xiannian Zhang, Linna Peng, Yingying Luo, Wenjia Guo, Jiacheng Yao, Mingming Shao, Wenyi Fan, Yamei Chen, Qionghua Cui, Yiyi Xi, Yanxia Sun, Xiangjie Niu, Xuan Zhao, Liping Chen, Yuqian Wang, Yachen Liu, Xinyu Yang, Chengcheng Wang, Ce Zhong, Wen Tan, Yanyi Huang, Jianbin Wang, Chen Wu, Dongxin Lin

Esophageal squamous-cell carcinoma (ESCC), one of the most prevalent and lethal malignant disease, has a complex but unknown tumor ecosystem. Here, we decipher for the first time the full compositions of ESCC tumor based on analyzing 208,659 single-cell transcriptomes in ESCC derived from 60 individuals. We identify 8 essential expression programs from malignant epithelial cells and discovered 43 cell types including 26 immune cell and 17 nonimmune stromal cell subtypes in the tumor microenvironment (TME), and also explicate the interactions between cancer cells and other cells and the interactions among different cell types in the TME. Moreover, we have linked the cancer cell transcriptomes to the somatic mutations and identified several markers significantly associated with survival time in patients, which may be relevant to precision cares of ESCC patients. These results renew our understanding of ESCC and provide a valuable example and resource for investigating other types of solid tumor.

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Species: human
Number of cells: 111028
Number of downloads: 10
Study size: 3GB
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Immunology 
immuno-oncology 
tumor microenvironment 
Immuno-suppressive 
Esophageal cancer 
Esophageal squamous-cell carcinoma 
Esophagus 

Dissecting esophageal squamous-cell carcinoma ecosystem by single-cell transcriptomic analysis (CD45 positive)

Xiannian Zhang, Linna Peng, Yingying Luo, Wenjia Guo, Jiacheng Yao, Mingming Shao, Wenyi Fan, Yamei Chen, Qionghua Cui, Yiyi Xi, Yanxia Sun, Xiangjie Niu, Xuan Zhao, Liping Chen, Yuqian Wang, Yachen Liu, Xinyu Yang, Chengcheng Wang, Ce Zhong, Wen Tan, Yanyi Huang, Jianbin Wang, Chen Wu, Dongxin Lin

Esophageal squamous-cell carcinoma (ESCC), one of the most prevalent and lethal malignant disease, has a complex but unknown tumor ecosystem. Here, we decipher for the first time the full compositions of ESCC tumor based on analyzing 208,659 single-cell transcriptomes in ESCC derived from 60 individuals. We identify 8 essential expression programs from malignant epithelial cells and discovered 43 cell types including 26 immune cell and 17 nonimmune stromal cell subtypes in the tumor microenvironment (TME), and also explicate the interactions between cancer cells and other cells and the interactions among different cell types in the TME. Moreover, we have linked the cancer cell transcriptomes to the somatic mutations and identified several markers significantly associated with survival time in patients, which may be relevant to precision cares of ESCC patients. These results renew our understanding of ESCC and provide a valuable example and resource for investigating other types of solid tumor.

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