Project description:Hidradenitis suppurativa (HS) is a highly prevalent, morbid inflammatory skin disease with limited treatment options. The major cell types and inflammatory pathways in skin of HS patients are poorly understood. We profiled via scRNASeq myeloid cells and keratinocytes sort-purified from two healthy skin samples and two samples with HS pathology to determine major cell types and transcriptional pathways altered in HS.
Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. Identifying transcriptional alterations within non-immune populations of HS lesions versus healthy controls could identify novel targets for therapy. We profiled subsets sorted as live, CD45 negative cells from biopsies of inflammatory lesions of three patients with HS and six specimens from healthy controls to determine what cell types and pathways were altered in HS inflammatory lesions.
Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. We and others have previously identified an abnormal B cell infiltrate within HS lesional skin. We performed scRNASequencing on CD3 negative cells from inflammatory HS skin lesions, healthy control skin and matched blood to better understand infiltrating B cells amongst other immune cells within lesional skin.
Project description:We performed scRNAseq analysis of CD45- cells sorted from murine brains on the presence or absence of a fluorescent reporter for complement component C3 at peak of experimental autoimmune encephalomyelitis to study the non-immune cellular sources of C3
Project description:The deficiency in CCL17 decreased atherosclerotic plaque burden by facilitating Treg maintenance and survival. cDC-derived CCL17 plays a crucial role in the recruitment and migration of various T cell subsets, including a subpopulation of CD4+ T cells, regulatory T cells (Tregs). To evaluate whether CCL17-deficient cDCs harbor an unique expression profile. we FACS-sorted CD45+CD11c+CD3-CD19- cells from lymph nodes (LNs) of Apoe-/-Ccl17wt/e or Apoe-/-Ccl17e/e mice on chew diet (CD) and performed single cell RNA sequencing (scRNAseq). We also performed scRNAseq to detect the expression of some chemokine receptors in sorted CD45+CD19-MHC+ cells from aortic LNs of Apoe-/-Ccl17wt/e or Apoe-/-Ccl17e/e mice on 6-week western diet (WD).
Project description:Exploration of proteome differences between CD45+ and CD45- cell types in renal cell carcinoma tumors and normal adjacent tissue patient samples.
Project description:Chimeric antigen receptor T cell (CAR-T) targeting the CD19 antigen represents an innovative therapeutic approach to improve the outcome of relapsed or refractory B-cell acute lymphoblastic leukemia (B-ALL). Yet, despite a high initial remission rate, CAR-T therapy ultimately fails for some patients. Notably, around half of relapsing patients develop CD19 negative (CD19neg) B-ALL allowing leukemic cells to evade CD19-targeted therapy. Herein, we investigate leukemic cells of a relapsing B-ALL patient, at two-time points: before (T1) and after (T2) anti-CD19 CAR-T treatment. We show that at T2, the B-ALL relapse is CD19 negative due to the expression of a non-functional CD19 transcript retaining intron 2. Then, using single-cell RNA sequencing (scRNAseq) approach, we demonstrate that CD19neg leukemic cells were present before CAR-T cell therapy and thus that the relapse results from the selection of these rare CD19neg B-ALL clones. In conclusion, our study shows that scRNAseq profiling can reveal pre-existing CD19neg subclones, raising the possibility to assess the risk of targeted therapy failure.
Project description:To delineate the potential molecular mechanisms underlying the communication between neutrophils and NK cells, we performed scRNAseq of the neutropenic bone marrow (12 months after transplantation of Cebpacre/+ Sbds +/+ or F/F cells). To this end, bone marrow cells were subsorted into HSC+MPP (LKS CD48-), HPC1 (LKS CD48+CD150-), B and T cells (B220+, CD3+), NK cells (NK1.1+ NKp46+) and a myeloid ‘rest’ fraction (B220-,CD3-,NKp46- and NK1.1-) and sorted fractions pooled together to obtain robust representation of all bone marrow cell types in the scRNAseq data