EBI2 regulates CXCL13‐mediated responses by heterodimerization with CXCR5

B‐cell movement into lymphoid follicles depends on the expression of the chemokine receptor CXCR5 and the recently reported Epstein‐Barr virus‐induced receptor 2 (EBI2). In cooperation with CXCR5, EBI2 helps to position activated B cells in the follicle, although the mechanism is poorly understood. Using human HEK293T cells and fluorescence resonance energy transfer (FRET) techniques, we demonstrate that CXCR5 and EBI2 form homo‐ and heterodimers. EBI2 expression modulated CXCR5 homodimeric complexes, as indicated by the FRET50 value (CXCR5 homodimer, 0.9851±0.0784; CXCR5 homodimer+EBI2, 1.7320±0.4905; P