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Type: Journal article
Title: Atypical chemokine receptor 4 shapes activated B cell fate
Author: Kara, E.
Bastow, C.
McKenzie, D.
Gregor, C.
Fenix, K.
Babb, R.
Norton, T.
Zotos, D.
Rodda, L.
Hermes, J.
Bourne, K.
Gilchrist, D.
Nibbs, R.
Alsharifi, M.
Vinuesa, C.
Tarlinton, D.
Brink, R.
Hill, G.
Cyster, J.
Comerford, I.
et al.
Citation: Journal of Experimental Medicine, 2018; 215(3):801-813
Publisher: Rockefeller University Press
Issue Date: 2018
ISSN: 0022-1007
Statement of
Ervin E. Kara, Cameron R. Bastow, Duncan R. McKenzie, Carly E. Gregor, Kevin A. Fenix, Rachelle Babb, Todd S. Norton, Dimitra Zotos, Lauren B. Rodda, Jana R. Hermes, Katherine Bourne, Derek S. Gilchrist, Robert J. Nibbs, Mohammed Alsharifi, Carola G. Vinuesa, David M. Tarlinton, Robert Brink, Geoffrey R. Hill, Jason G. Cyster, Iain Comerford, and Shaun R. McColl
Abstract: 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.
Keywords: Germinal Center; Spleen; B-Lymphocytes; Animals; Mice, Inbred C57BL; Antigens; Cell Proliferation; Cell Lineage; Receptors, CCR
Description: Published Online: 31 January, 2018
Rights: © 2018 Kara et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see After six months it is available under a Creative Commons License (Attribution–Noncommercial– Share Alike 4.0 International license, as described at
RMID: 0030081339
DOI: 10.1084/jem.20171067
Grant ID:
Appears in Collections:Molecular and Biomedical Science publications

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