{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Jon Sicilia"],"organism":["Mus musculus"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16912"],"description":["This study investigates the role of dendritic cells (DCs) in anti-tumor immunity, focusing on the phosphatase SHP-1 and its regulation of signaling pathways and interactions with CD8+ T cells. Using conditional knockout mouse models and single-cell transcriptomics, we show that SHP-1 loss in conventional type 1 dendritic cells (cDC1s) and macrophages disrupts interferon responses, antigen presentation, and migratory programs, leading to impaired tumor rejection and reduced efficacy of PD-1 blockade. These findings provide mechanistic insights into dendritic cell biology within the tumor microenvironment (TME) and identify SHP-1 as a key regulator with implications for the design of DC-based cancer immunotherapies."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Library Construction - For each sample, 40,000 cells were loaded into a BD Rhapsody Single Cell Analysis System cartridge. After cell capture, lysis, and mRNA capture on barcoded beads, cDNA synthesis was performed according to the manufacturer’s instructions. Independent indexed whole-transcriptome libraries were then prepared for each sample. Library size was assessed using an Agilent 2100 Bioanalyzer and concentration was measured with a Qubit fluorometer.","Sample Collection - Subcutaneous MC38 tumors were generated in female mice and harvested on day 12 after tumor inoculation. Tumors from five mice per genotype were pooled, mechanically dissociated, and enzymatically digested with 0.5 mg/mL collagenase IV and 0.2 mg/mL DNase I for 1 hour at 37°C. Single-cell suspensions were filtered, red blood cells were lysed, and CD11c+ tumor-infiltrating cells were enriched by magnetic positive selection and subsequently FACS-sorted before single-cell RNA-seq.","Nucleic Acid Extraction - No separate bulk RNA extraction was performed. Purified viable CD11c+ cells were loaded directly into the BD Rhapsody Single Cell Analysis System, where individual cells were captured in nanowells, lysed, and released mRNA was captured on barcoded beads for downstream cDNA synthesis.","Sequencing - Indexed libraries were pooled and sequenced in paired-end mode (51 × 75 bp) on an Illumina NextSeq 2000 using a P3 flow cell. Base calling and run processing were performed with NextSeq 1000/2000 Control Software Suite v1.4.1, and FASTQ files were generated using BCL Convert v3.6.3. Raw FASTQ files were processed with BD Rhapsody pipeline v2.2 and aligned to the mouse mm10 reference genome (RhapRef_Mouse_WTA_2023-02"],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Data Transformation - No normalization or data transformation was applied to the submitted data. Raw sequencing data (FASTQ files) are provided, together with gene expression count matrices generated by the BD Rhapsody analysis pipeline. These matrices represent raw counts per cell and have not been further normalized or transformed."],"omics_type":["Unknown","Transcriptomics"],"instrument_platform":["NextSeq 2000"],"study_type":["RNA-seq of coding RNA from single cells"],"species":["Mus musculus"],"pubmed_title":["Loss of SHP-1 in CD11c+ cells impairs anti-tumor immunity"],"pubmed_authors":["Pablo Munné de Juan","Jon Sicilia","Miguel Galán , Elena Hernández-García , Pablo Munné , Ana Redondo-Urzainqui , Francisco J Cueto , Jon Sicilia , Sergio Callejas Alejano , M Ascensión Rey-Martín , Ana Dopazo , David Sancho  and Salvador Iborra"],"additional_accession":[]},"is_claimable":false,"name":"scRNA-seq of tumor infiltrating CD11c + cells in ItgaxΔPtpn6 model","description":"This study investigates the role of dendritic cells (DCs) in anti-tumor immunity, focusing on the phosphatase SHP-1 and its regulation of signaling pathways and interactions with CD8+ T cells. Using conditional knockout mouse models and single-cell transcriptomics, we show that SHP-1 loss in conventional type 1 dendritic cells (cDC1s) and macrophages disrupts interferon responses, antigen presentation, and migratory programs, leading to impaired tumor rejection and reduced efficacy of PD-1 blockade. These findings provide mechanistic insights into dendritic cell biology within the tumor microenvironment (TME) and identify SHP-1 as a key regulator with implications for the design of DC-based cancer immunotherapies.","dates":{"release":"2026-04-15T00:00:00Z","modification":"2026-04-15T17:08:24.494Z","creation":"2026-04-15T17:07:50.013Z"},"accession":"E-MTAB-16912","cross_references":{"ENA":["ERP192196"],"EFO":["EFO_0002944","EFO_0004170","EFO_0005684","EFO_0005518","EFO_0003816","EFO_0004184"]}}