Figure 1
From: Subversion of the B-cell compartment during parasitic, bacterial, and viral infections
Differentiation and trafficking of innate and follicular B-cells. Mouse, and probably human, B-1 cells home to the serous cavities in steady state conditions and migrate to the spleen after activation by pathogens where they differentiate into natural Immunoglobulin (Ig) M-producing cells. Follicular (FO) B-cells are produced from bone marrow precursors that mature sequentially into pro-B and pre-B cells (not detailed) and immature mIgM+ B-cells. Immature-transitional 1 (Trans 1) B-cells migrate through the blood into spleen marginal zone (MZ) where they mature into transitional 2 (Trans 2) B-cells. Based on the balance between BCR-Notch2 signals, they next differentiate into FO or MZ B-cells. MZ B cells secrete low affinity IgM after antigenic stimulation. In the germinal center (GC), FO helper T-cells (TFH) support the selection and survival of B-cell clones with high-affinity BCR. Once selected, these clones differentiate into two types of effector cells, memory B-cells (Mem B) and plasma cell precursors (plasmablasts, PBl), and leave the spleen. The PBl migrate into the bone marrow and constitute a pool of long-lived plasma cells producing high-affinity Ig, whereas the Mem B migrate into extra-follicular areas in secondary lymphoid tissues.