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BOB.1 controls memory B-cell fate in the germinal center reaction. / Levels, Maartje J.; Fehres, Cynthia M.; van Baarsen, Lisa G. M.; van Uden, Nathalie O. P.; Germar, Kristine; O'Toole, Tom G.; Blijdorp, Iris C. J.; Semmelink, Johanna F.; Doorenspleet, Marieke E.; Bakker, Arjen Q.; Krasavin, Mikhail; Tomilin, Alexey; Brouard, Sophie; Spits, Hergen; Baeten, Dominique L. P.; Yeremenko, Nataliya G.

In: Journal of Autoimmunity, Vol. 101, 07.2019, p. 131-144.

Research output: Contribution to journal › Article › peer-review

Harvard

Levels, MJ, Fehres, CM, van Baarsen, LGM, van Uden, NOP, Germar, K, O'Toole, TG, Blijdorp, ICJ, Semmelink, JF, Doorenspleet, ME, Bakker, AQ, Krasavin, M, Tomilin, A, Brouard, S, Spits, H, Baeten, DLP & Yeremenko, NG 2019, 'BOB.1 controls memory B-cell fate in the germinal center reaction', Journal of Autoimmunity, vol. 101, pp. 131-144. https://doi.org/10.1016/j.jaut.2019.04.011

APA

Levels, M. J., Fehres, C. M., van Baarsen, L. G. M., van Uden, N. O. P., Germar, K., O'Toole, T. G., Blijdorp, I. C. J., Semmelink, J. F., Doorenspleet, M. E., Bakker, A. Q., Krasavin, M., Tomilin, A., Brouard, S., Spits, H., Baeten, D. L. P., & Yeremenko, N. G. (2019). BOB.1 controls memory B-cell fate in the germinal center reaction. Journal of Autoimmunity, 101, 131-144. https://doi.org/10.1016/j.jaut.2019.04.011

Vancouver

Levels MJ, Fehres CM, van Baarsen LGM, van Uden NOP, Germar K, O'Toole TG et al. BOB.1 controls memory B-cell fate in the germinal center reaction. Journal of Autoimmunity. 2019 Jul;101:131-144. https://doi.org/10.1016/j.jaut.2019.04.011

Author

Levels, Maartje J. ; Fehres, Cynthia M. ; van Baarsen, Lisa G. M. ; van Uden, Nathalie O. P. ; Germar, Kristine ; O'Toole, Tom G. ; Blijdorp, Iris C. J. ; Semmelink, Johanna F. ; Doorenspleet, Marieke E. ; Bakker, Arjen Q. ; Krasavin, Mikhail ; Tomilin, Alexey ; Brouard, Sophie ; Spits, Hergen ; Baeten, Dominique L. P. ; Yeremenko, Nataliya G. / BOB.1 controls memory B-cell fate in the germinal center reaction. In: Journal of Autoimmunity. 2019 ; Vol. 101. pp. 131-144.

BibTeX

@article{746ba04b8a0a411a8ec92874944cb5de,
title = "BOB.1 controls memory B-cell fate in the germinal center reaction",
abstract = "During T cell-dependent (TD) germinal center (GC) responses, naive B cells are instructed to differentiate towards GC B cells (GCBC), high-affinity long-lived plasma cells (LLPC) or memory B cells (Bmem). Alterations in the B cell-fate choice could contribute to immune dysregulation leading to the loss of self-tolerance and the initiation of autoimmune disease. Here we show that mRNA levels of the transcription regulator BOB.1 are increased in the lymph node compartment of patients with rheumatoid arthritis (RA), a prototypical auto immune disease caused by the loss of immunological tolerance. Investigating to what extent levels of BOB.1 impact B cells during TD immune responses we found that BOB.1 has a crucial role in determining the B cell-fate decision. High BOB.1 levels promote the generation of cells with phenotypic and functional characteristics of Bmem. Mechanistically, overexpression of BOB.1 drives ABFI and suppresses BCL6, favouring Bmem over LLPC or recycling GCBC. Low levels of BOB.1 are sufficient for LLPC but not for Bmem differentiation. Our findings demonstrate a novel role for BOB.1 in B cells during TD GC responses and suggest that its dysregulation may contribute to the pathogenesis of RA by disturbing the B cell-fate determination.",
keywords = "Autoimmune disease, Rheumatoid arthritis, BOB.1, Germinal center, B cell, Memory B cell, PLASMA-CELL, ANTIGEN RECEPTOR, UP-REGULATION, OCA-B, IMMUNE-RESPONSE, LYMPH-NODES, DIFFERENTIATION, COACTIVATOR, TRANSCRIPTION, AFFINITY",
author = "Levels, {Maartje J.} and Fehres, {Cynthia M.} and {van Baarsen}, {Lisa G. M.} and {van Uden}, {Nathalie O. P.} and Kristine Germar and O'Toole, {Tom G.} and Blijdorp, {Iris C. J.} and Semmelink, {Johanna F.} and Doorenspleet, {Marieke E.} and Bakker, {Arjen Q.} and Mikhail Krasavin and Alexey Tomilin and Sophie Brouard and Hergen Spits and Baeten, {Dominique L. P.} and Yeremenko, {Nataliya G.}",
year = "2019",
month = jul,
doi = "10.1016/j.jaut.2019.04.011",
language = "Английский",
volume = "101",
pages = "131--144",
journal = "Journal of Autoimmunity",
issn = "0896-8411",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - BOB.1 controls memory B-cell fate in the germinal center reaction

AU - Levels, Maartje J.

AU - Fehres, Cynthia M.

AU - van Baarsen, Lisa G. M.

AU - van Uden, Nathalie O. P.

AU - Germar, Kristine

AU - O'Toole, Tom G.

AU - Blijdorp, Iris C. J.

AU - Semmelink, Johanna F.

AU - Doorenspleet, Marieke E.

AU - Bakker, Arjen Q.

AU - Krasavin, Mikhail

AU - Tomilin, Alexey

AU - Brouard, Sophie

AU - Spits, Hergen

AU - Baeten, Dominique L. P.

AU - Yeremenko, Nataliya G.

PY - 2019/7

Y1 - 2019/7

N2 - During T cell-dependent (TD) germinal center (GC) responses, naive B cells are instructed to differentiate towards GC B cells (GCBC), high-affinity long-lived plasma cells (LLPC) or memory B cells (Bmem). Alterations in the B cell-fate choice could contribute to immune dysregulation leading to the loss of self-tolerance and the initiation of autoimmune disease. Here we show that mRNA levels of the transcription regulator BOB.1 are increased in the lymph node compartment of patients with rheumatoid arthritis (RA), a prototypical auto immune disease caused by the loss of immunological tolerance. Investigating to what extent levels of BOB.1 impact B cells during TD immune responses we found that BOB.1 has a crucial role in determining the B cell-fate decision. High BOB.1 levels promote the generation of cells with phenotypic and functional characteristics of Bmem. Mechanistically, overexpression of BOB.1 drives ABFI and suppresses BCL6, favouring Bmem over LLPC or recycling GCBC. Low levels of BOB.1 are sufficient for LLPC but not for Bmem differentiation. Our findings demonstrate a novel role for BOB.1 in B cells during TD GC responses and suggest that its dysregulation may contribute to the pathogenesis of RA by disturbing the B cell-fate determination.

AB - During T cell-dependent (TD) germinal center (GC) responses, naive B cells are instructed to differentiate towards GC B cells (GCBC), high-affinity long-lived plasma cells (LLPC) or memory B cells (Bmem). Alterations in the B cell-fate choice could contribute to immune dysregulation leading to the loss of self-tolerance and the initiation of autoimmune disease. Here we show that mRNA levels of the transcription regulator BOB.1 are increased in the lymph node compartment of patients with rheumatoid arthritis (RA), a prototypical auto immune disease caused by the loss of immunological tolerance. Investigating to what extent levels of BOB.1 impact B cells during TD immune responses we found that BOB.1 has a crucial role in determining the B cell-fate decision. High BOB.1 levels promote the generation of cells with phenotypic and functional characteristics of Bmem. Mechanistically, overexpression of BOB.1 drives ABFI and suppresses BCL6, favouring Bmem over LLPC or recycling GCBC. Low levels of BOB.1 are sufficient for LLPC but not for Bmem differentiation. Our findings demonstrate a novel role for BOB.1 in B cells during TD GC responses and suggest that its dysregulation may contribute to the pathogenesis of RA by disturbing the B cell-fate determination.

KW - Autoimmune disease

KW - Rheumatoid arthritis

KW - BOB.1

KW - Germinal center

KW - B cell

KW - Memory B cell

KW - PLASMA-CELL

KW - ANTIGEN RECEPTOR

KW - UP-REGULATION

KW - OCA-B

KW - IMMUNE-RESPONSE

KW - LYMPH-NODES

KW - DIFFERENTIATION

KW - COACTIVATOR

KW - TRANSCRIPTION

KW - AFFINITY

U2 - 10.1016/j.jaut.2019.04.011

DO - 10.1016/j.jaut.2019.04.011

M3 - статья

VL - 101

SP - 131

EP - 144

JO - Journal of Autoimmunity

JF - Journal of Autoimmunity

SN - 0896-8411

ER -

ID: 50700728