| First Author | Yi T | Year | 2013 |
| Journal | Elife | Volume | 2 |
| Pages | e00757 | PubMed ID | 23682316 |
| Mgi Jnum | J:198681 | Mgi Id | MGI:5498633 |
| Doi | 10.7554/eLife.00757 | Citation | Yi T, et al. (2013) EBI2-mediated bridging channel positioning supports splenic dendritic cell homeostasis and particulate antigen capture. Elife 2:e00757 |
| abstractText | Splenic dendritic cells (DCs) present blood-borne antigens to lymphocytes to promote T cell and antibody responses. The cues involved in positioning DCs in areas of antigen exposure in the spleen are undefined. Here we show that CD4(+) DCs highly express EBI2 and migrate to its oxysterol ligand, 7alpha,25-OHC. In mice lacking EBI2 or the enzymes needed for generating normal distributions of 7alpha,25-OHC, CD4(+) DCs are reduced in frequency and the remaining cells fail to situate in marginal zone bridging channels. The CD4(+) DC deficiency can be rescued by LTbetaR agonism. EBI2-mediated positioning in bridging channels promotes DC encounter with blood-borne particulate antigen. Upon exposure to antigen, CD4(+) DCs move rapidly to the T-B zone interface and promote induction of helper T cell and antibody responses. These findings establish an essential role for EBI2 in CD4(+) DC positioning and homeostasis and in facilitating capture and presentation of blood-borne particulate antigens. DOI:http://dx.doi.org/10.7554/eLife.00757.001. |
