The inhibitory receptor Siglec-G controls the severity of chronic lymphocytic leukemia
Chronic Lymphocytic Leukaemia (CLL) is the most common leukemia in adults in the Western world. B cell receptor (BCR) signalling is known to be crucial for the pathogenesis and maintenance of CLL cells develop from mature CD5+ B cells. BCR signalling is regulated by the inhibitory co-receptor Siglec-G and Siglec-G-deficient mice have an enlarged CD5+ B1a cell population. Here, we determine how Siglec-G expression influences the severity of CLL. Overall design: Immunoglobulin specific repertoire analysis of murine B cell receptor heavy chain Samples were collected by drawing blood at the age of 12, 24, 36 and 48 weeks for TCL1, TCL1 x Siglecg-/- mice and their corresponding controls and at the age of 28, 36 and 48 weeks for TCL1 x Siglecg-R26ki/ki and TCL1 x Siglecg-R26ki/ki x mb1cre mice and controls. Then CD19+ B cells were sorted. The igblast output data consists of reads of antibodies created from mRNA with UMIs and annotated to the germline reference, which are listed in v_call, d_call, j_call columns and are already normalised with unique UMIs to single mRNA molecules. The first sequence ID column contains the header from the normalised fasta files: 1|IgA|CTGCAAAAGTAGAGGTTGAG-9 UniqueNumber|Isotype|UMI|-UMIcount The last number in the header after the dash is UMI abundance/unique read count. For BCRseq research in this case only unique mRNA molecule are relevant for fidelity (in contrast to bulk RNAseq where read counts of multiple genes are compared to evaluate expression levels).