Project description:IgG cytoplasmic tail interferes with the induction of antigen-response genes Experiment Overall Design: Comparing antigen-induced genes between B cells expressing anti-HEL IgM BCR and IgMG BCR (chimeric receptor where the extracellular spacer, transmembrane, and cytoplasmic domain of IgM are replaced with those of IgG1)
Project description:Although immunoglobulin class-switching from IgM to IgG enhances B cell receptor (BCR) signalling and antibody responses, certain subsets of B cell lymphomas retain unswitched IgM BCRs despite signs of class-switching in the immunoglobulin heavy chain loci. This suggests that expression of the IgG BCR suppresses progression of specific lymphoma subsets. We found that inducing BCR class switching from IgM to IgG1 or IgG4 inhibits proliferation of EZB DLBCL lymphoma cell lines. To understand changes associated with class-switching we compared transcritional profiles of isogenic WSU-FSCCL and NU-DHL1 cell lines artificially class-switched to express IgM and IgG1 BCRs. In addition, we analysed transcriptional profiles of IgG1+ cell lines into which we introduced the IgG1 W375* mutation that truncates the intracellular IgG tail.
