Oncogenic Calreticulin Induces Immune Escape by Stimulating TGF-ß Expression and Regulatory T Cell Expansion in the Bone Marrow Microenvironment - scRNAseq
We established a model for myeloproliferative disease in mice, that is based on primary bone marrow expressing human Thrombopoietin receptor and human mutant Calrdel52. To learn more about cellular and transcriptional rearrangements in the bone marrow we performed single cell RNA sequencing comparing bone marrow cells of empty vector control mice with mice that received MPL-Calrdel52 bone marrow. Overall design: A total of two mice for each group were analyzed. Two Mice received empty vector control BM. Two mice received MPL-Calr(del52) BM. Vector included an IRES-GFP sequence as transduction/engraftment control. Engraftment and disease phenotype was checked before analysis.