Abstract
Abstract The ubiquitously expressed transcription factor TFII-I is a multifunctional protein with pleiotropic roles in gene regulation and, germline deletion of the Gtf2i gene leads to embryonic lethality. To delineate the physiological role of TFII-I in murine B cells, we carried out conditional deletion of Gtf2i. Here we report a surprising phenotype that suggests a role for TFII-I in homeostasis of innate properties of B lymphocytes. B cell transcriptome and chromatin landscape is skewed towards myeloid like features in the absence of TFII-I. Gtf2i ablated B cells also demonstrate enhanced sensitivity towards LPS induced transcription and proliferative capacities, features associated with innate immune cells. Finally, increased IgG3 switching, which is normally associated with inflammation, was observed in the absence of TFII-I. These results suggest an unexpected role for TFII-I in maintaining immune homeostasis and provide further clues for GTF2I polymorphism associated with B cell dominated autoimmune diseases. This work was supported in part by the intramural program of the NIH, National Institute on Aging (NIA)
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