FDCs, in turn, attract B cells with chemoattractant CXCL13. B cells lacking CXCR5, the receptor for CXCL13, still enter the white pulp, but are mislocalized and disorganized. To generate follicular structures, FDCs need to be stimulated by lymphotoxin (LT), a mediator produced by B cells. The stimulation of CXCR5 on B cells upregulates LT production, which leads to FDCs activation and stimulates further CXCL13 secretion, thus generating a positive feed-forward loop. This results in the formation of GC, where antigen-activated B cells are trapped to undergo somatic mutation, positive and negative selection, isotype switching, and differentiation into high-affinity plasma cells and memory B cells. Adhesion between FDCs and B cells is mediated by ICAM-1 (CD54)–LFA-1 (CD11a) and VCAM–VLA-4 molecules.