KLF2, a master regulator of peripheral B lymphocyte homeostasis

Lymphocytes play a prominent role in the combat of infectious diseases. For a sufficient but limited immune response it is essential that migration and activation of lymphocytes are strictly controlled. The transcription factor KLF2 modulates T lymphocyte egress from lymphoid organs by regulating S1P1. This is not the case for B cells. Instead, KLF2 regulates homeostasis of B cells in peripheral lymphatic organs and homing of plasma cells to the bone marrow, presumably by controlling the expression of beta7 integrin. In mice with a B cell-specific deletion of KLF2, S1P1 expression on B cells was only slightly affected. Accordingly, all splenic B cell subsets were present, but their numbers were increased with a clear bias for marginal zone (MZ) B cells. In contrast, fewer peyers patches harboring less B cells, fewer B1 cells in the peritoneal cavity as well as recirculating B cells in the bone marrow were found. Upon thymus-dependent immunization, IgG titers were diminished and antigen-specific plasma cells were absent in the bone marrow. Furthermore this study provides first evidence that KLF2 is posttranslationally phosphorylated directly or indirectly by the PI3K signaling pathway.

Autorentext

Rebecca Winkelmann, born 1982 in Kleve, received her diploma in Molecular Medicine from the University of Erlangen-Nürnberg in 2007. She graduated as Dr. rer. nat. on the role of KLF2 in B cells in 2010. Currently, she is working as a postdoctoral fellow in the group of Prof. Dr. Hans-Martin Jäck at the Division of Molecular Immunology in Erlangen.