Importantly, IL-17 cytokines coordinate the timely sequestration of responder B cells within the follicular light zone of germinal centers (GC), via upregulation of the regulators of G-protein signals (RGS) Rgs13 and Rgs16, thus suppressing B cell’s chemotactic response to CXCL12 and CXCL13, and ensuring their interaction with follicular Th cells to promote B cell differentiation into autoantibody-producing plasma B cells in a RA BXD2 mice model [21], [28]. The gene discussed is CXCL13; the disease is rheumatoid arthritis.