Helper T cells move to the interface of the T cell zone and B cell follicles shortly after activation, a relocation event that is important for their ability to support T cell-dependent antibody responses. While CXCR5 is well established to play a critical role in promoting T cell entry into follicles, the guidance mechanisms responsible for T cell positioning at the B-T zone interface have been less understood. EBI2 (GPR183) is a chemoattractant receptor that responds to the oxysterol 7a,25-dihydroxycholesterol (7a,25-HC) and guides the movements of activated B cells. We recently found that EBI2 is unregulated on activated CD4 T cells and promotes their movement to the B-T zone interface in response to 7a,25-HC. As well as promoting interactions between cognate T cells and B cells, we find that this positioning fosters interactions with activated CD4+DCIR2+ dendritic cells (cDC2s). Positioning of sentinel cDC2s in the spleen is found to require the action of two EBI2 ligands, 7a,25-HC and 7a,27-HC. Following activation by certain stimuli, cDC2s rapidly migrate to the B-T zone interface. This occurs due to upregulation of both CCR7 and EBI2 and the integrated action of these two chemoattractant receptors. Our work on the requirements for EBI2 ligand production led us to identify a role for the precursor oxysterol, 25-HC, in regulation of macrophage sterol metabolism, inflammasome activation and IL-1b production. In ongoing work we are studying how 25-HC influences macrophage metabolism in a way that limits inflammasome activation. We are also testing whether 25-HC acts as an intercellular communication molecule to regulate the metabolic state of responder cells. Our ongoing work in these areas will be presented.