Master of Science
Microbiology and Immunology
DeKoter, Rodney P.
The activation of B cells culminates in a fate decision between plasma cell or memory B cell differentiation pathways. Mice lacking the Ets transcription factor Spi-B exhibit impaired secondary antibody (Ab)-forming responses. The role of the related factor Spi-C in Ab-forming responses remains unknown. Using Spib-/-Spic+/- mice, we showed that heterozygosity of Spi-C rescued reductions in secondary IgG1-secreting cell frequencies. Spib-/- and Spib-/-Spic+/- B cells generated increased frequencies of CD138+ cells, relative to WT B cells. Spib-/- B cells underwent accelerated differentiation compared to WT B cells, while Spib-/-Spic+/- B cells exhibited a lag in differentiation. Gene expression analysis indicated that Bach2 was downregulated in CD138+ Spib-/- cells. ChIP experiments suggested that Spi-B and Spi-C were enriched at Ets binding sites located within Bach2 in stimulated B cells. Our results point to a novel role for Spi-C in opposing the function of Spi-B in activated B cells.
Laramee, Anne-Sophie, "Counteracting Roles for the Related E26 Transformation Specific Transcription Factors Spi-B and Spi-C in Regulating Antibody-Forming Responses" (2018). Electronic Thesis and Dissertation Repository. 5476.