Assessing the role of the T-box transcription factor Eomes in B cell differentiation during either Th1 or Th2 cell-biased responses

• Published in: PloS one 2018-12, Vol.13 (12), p.e0208343-e0208343
• Main Authors: Cooper, Lucy, Hailes, Lauren, Sheikh, Amania, Zaph, Colby, Belz, Gabrielle T, Groom, Joanna R, Good-Jacobson, Kim L
• Format: Article
• Language: English
• Subjects: Analysis; Animals; Antibodies; Antiviral agents; B cells; B-Lymphocytes - cytology; B-Lymphocytes - metabolism; Biochemistry; Biology and Life Sciences; CD8 antigen; Cell differentiation; Cell Differentiation - genetics; Cell Differentiation - physiology; Clonal deletion; Differentiation (biology); DNA binding proteins; Flow cytometry; Germinal centers; Helper cells; Immune response; Immunological memory; Infections; Influenza; Lymphocyte Activation; Lymphocytes; Lymphocytes B; Lymphocytes T; Medical research; Medicine and Health Sciences; Memory cells; Mice; Molecular biology; Pathogenic microorganisms; Plasma cells; T cells; T-Box Domain Proteins - genetics; T-Box Domain Proteins - metabolism; Th1 Cells - metabolism; Th2 Cells - metabolism; Transcription factors; Vaccination; Viral infections; Virology
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0208343

Successful T-dependent humoral responses require the production of antibody-secreting plasmablasts, as well as the formation of germinal centers which eventually form high-affinity B cell memory. The ability of B cells to differentiate into germinal center and plasma cells, as well as the ability to tailor responses to different pathogens, is driven by transcription factors. In T cells, the T-box transcription factors T-bet and Eomesodermin (Eomes) regulate effector and memory T cell differentiation, respectively. While T-bet has a critical role in regulating anti-viral B cell responses, a role for Eomes in B cells has yet to be described. We therefore investigated whether Eomes was required for B cell differentiation during either Th1 or Th2 cell-biased immune responses. Here, we demonstrate that deletion of Eomes specifically in B cells did not affect B cell differentiation in response to vaccination, as well as following viral or helminth infection. In contrast to its established role in CD8+ T cells, Eomes did not influence memory B cell differentiation. Finally, the use of an Eomes reporter mouse confirmed the lack of Eomes expression during immune responses. Thus, germinal center and plasma cell differentiation and the formation of isotype-switched memory B cells in response to infection are independent of Eomes expression.