Marginal Zone Formation Requires ACKR3 Expression on B Cells
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Marginal Zone Formation Requires ACKR3 Expression on B Cells. / Radice, Egle; Ameti, Rafet; Melgrati, Serena; Foglierini, Mathilde; Antonello, Paola; Stahl, Rolf A K; Thelen, Sylvia; Jarrossay, David; Thelen, Marcus.
In: CELL REP, Vol. 32, No. 5, 04.08.2020, p. 107951.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Marginal Zone Formation Requires ACKR3 Expression on B Cells
AU - Radice, Egle
AU - Ameti, Rafet
AU - Melgrati, Serena
AU - Foglierini, Mathilde
AU - Antonello, Paola
AU - Stahl, Rolf A K
AU - Thelen, Sylvia
AU - Jarrossay, David
AU - Thelen, Marcus
N1 - Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.
PY - 2020/8/4
Y1 - 2020/8/4
N2 - The marginal zone (MZ) contributes to the highly organized spleen microarchitecture. We show that expression of atypical chemokine receptor 3 (ACKR3) defines two equal-sized populations of mouse MZ B cells (MZBs). ACKR3 is required for development of a functional MZ and for positioning of MZBs. Deletion of ACKR3 on B cells distorts the MZ, and MZBs fail to deliver antigens to follicles, reducing humoral responses. Reconstitution of MZ-deficient CD19ko mice shows that ACKR3- MZBs can differentiate into ACKR3+ MZBs, but not vice versa. The lack of a MZ is rescued by adoptive transfer of ACKR3-sufficient, and less by ACKR3-deficient, follicular B cells (FoBs); hence, ACKR3 expression is crucial for establishment of the MZ. The inability of CD19ko mice to respond to T-independent antigen is rescued when ACKR3-proficient, but not ACKR3-deficient, FoBs are transferred. Accordingly, ACKR3-deficient FoBs are able to reconstitute the MZ if the niche is pre-established by ACKR3-proficient MZBs.
AB - The marginal zone (MZ) contributes to the highly organized spleen microarchitecture. We show that expression of atypical chemokine receptor 3 (ACKR3) defines two equal-sized populations of mouse MZ B cells (MZBs). ACKR3 is required for development of a functional MZ and for positioning of MZBs. Deletion of ACKR3 on B cells distorts the MZ, and MZBs fail to deliver antigens to follicles, reducing humoral responses. Reconstitution of MZ-deficient CD19ko mice shows that ACKR3- MZBs can differentiate into ACKR3+ MZBs, but not vice versa. The lack of a MZ is rescued by adoptive transfer of ACKR3-sufficient, and less by ACKR3-deficient, follicular B cells (FoBs); hence, ACKR3 expression is crucial for establishment of the MZ. The inability of CD19ko mice to respond to T-independent antigen is rescued when ACKR3-proficient, but not ACKR3-deficient, FoBs are transferred. Accordingly, ACKR3-deficient FoBs are able to reconstitute the MZ if the niche is pre-established by ACKR3-proficient MZBs.
U2 - 10.1016/j.celrep.2020.107951
DO - 10.1016/j.celrep.2020.107951
M3 - SCORING: Journal article
C2 - 32755592
VL - 32
SP - 107951
JO - CELL REP
JF - CELL REP
SN - 2211-1247
IS - 5
ER -