| First Author | Kara EE | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 3 | Pages | 801-813 |
| PubMed ID | 29386231 | Mgi Jnum | J:263057 |
| Mgi Id | MGI:6120380 | Doi | 10.1084/jem.20171067 |
| Citation | Kara EE, et al. (2018) Atypical chemokine receptor 4 shapes activated B cell fate. J Exp Med 215(3):801-813 |
| abstractText | Activated B cells can initially differentiate into three functionally distinct fates-early plasmablasts (PBs), germinal center (GC) B cells, or early memory B cells-by mechanisms that remain poorly understood. Here, we identify atypical chemokine receptor 4 (ACKR4), a decoy receptor that binds and degrades CCR7 ligands CCL19/CCL21, as a regulator of early activated B cell differentiation. By restricting initial access to splenic interfollicular zones (IFZs), ACKR4 limits the early proliferation of activated B cells, reducing the numbers available for subsequent differentiation. Consequently, ACKR4 deficiency enhanced early PB and GC B cell responses in a CCL19/CCL21-dependent and B cell-intrinsic manner. Conversely, aberrant localization of ACKR4-deficient activated B cells to the IFZ was associated with their preferential commitment to the early PB linage. Our results reveal a regulatory mechanism of B cell trafficking via an atypical chemokine receptor that shapes activated B cell fate. |
