Galectin-9 binds IgM-BCR to regulate B cell signaling

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Galectin-9 binds IgM-BCR to regulate B cell signaling. / Cao, Anh; Alluqmani, Nouf; Buhari, Fatima Hifza Mohammed; Wasim, Laabiah; Smith, Logan K.; Quaile, Andrew T.; Shannon, Michael; Hakim, Zaki; Furmli, Hossai; Owen, Dylan M.; Savchenko, Alexei; Treanor, Bebhinn.

In: Nature Communications, Vol. 9, No. 1, 3288, 01.12.2018.

Research output: Contribution to journalArticlepeer-review

Harvard

Cao, A, Alluqmani, N, Buhari, FHM, Wasim, L, Smith, LK, Quaile, AT, Shannon, M, Hakim, Z, Furmli, H, Owen, DM, Savchenko, A & Treanor, B 2018, 'Galectin-9 binds IgM-BCR to regulate B cell signaling', Nature Communications, vol. 9, no. 1, 3288. https://doi.org/10.1038/s41467-018-05771-8

APA

Cao, A., Alluqmani, N., Buhari, F. H. M., Wasim, L., Smith, L. K., Quaile, A. T., Shannon, M., Hakim, Z., Furmli, H., Owen, D. M., Savchenko, A., & Treanor, B. (2018). Galectin-9 binds IgM-BCR to regulate B cell signaling. Nature Communications, 9(1), [3288]. https://doi.org/10.1038/s41467-018-05771-8

Vancouver

Cao A, Alluqmani N, Buhari FHM, Wasim L, Smith LK, Quaile AT et al. Galectin-9 binds IgM-BCR to regulate B cell signaling. Nature Communications. 2018 Dec 1;9(1). 3288. https://doi.org/10.1038/s41467-018-05771-8

Author

Cao, Anh ; Alluqmani, Nouf ; Buhari, Fatima Hifza Mohammed ; Wasim, Laabiah ; Smith, Logan K. ; Quaile, Andrew T. ; Shannon, Michael ; Hakim, Zaki ; Furmli, Hossai ; Owen, Dylan M. ; Savchenko, Alexei ; Treanor, Bebhinn. / Galectin-9 binds IgM-BCR to regulate B cell signaling. In: Nature Communications. 2018 ; Vol. 9, No. 1.

Bibtex

@article{8fea3f60dd3b4759ad5df119546cc391,
title = "Galectin-9 binds IgM-BCR to regulate B cell signaling",
abstract = "The galectin family of secreted lectins have emerged as important regulators of immune cell function; however, their role in B-cell responses is poorly understood. Here we identify IgM-BCR as a ligand for galectin-9. Furthermore, we show enhanced BCR microcluster formation and signaling in galectin-9-deficient B cells. Notably, treatment with exogenous recombinant galectin-9 nearly completely abolishes BCR signaling. We investigated the molecular mechanism for galectin-9-mediated inhibition of BCR signaling using super-resolution imaging and single-particle tracking. We show that galectin-9 merges pre-existing nanoclusters of IgM-BCR, immobilizes IgM-BCR, and relocalizes IgM-BCR together with the inhibitory molecules CD45 and CD22. In resting naive cells, we use dual-color super-resolution imaging to demonstrate that galectin-9 mediates the close association of IgM and CD22, and propose that the loss of this association provides a mechanism for enhanced activation of galectin-9-deficient B cells.",
author = "Anh Cao and Nouf Alluqmani and Buhari, {Fatima Hifza Mohammed} and Laabiah Wasim and Smith, {Logan K.} and Quaile, {Andrew T.} and Michael Shannon and Zaki Hakim and Hossai Furmli and Owen, {Dylan M.} and Alexei Savchenko and Bebhinn Treanor",
year = "2018",
month = dec,
day = "1",
doi = "10.1038/s41467-018-05771-8",
language = "English",
volume = "9",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - Galectin-9 binds IgM-BCR to regulate B cell signaling

AU - Cao, Anh

AU - Alluqmani, Nouf

AU - Buhari, Fatima Hifza Mohammed

AU - Wasim, Laabiah

AU - Smith, Logan K.

AU - Quaile, Andrew T.

AU - Shannon, Michael

AU - Hakim, Zaki

AU - Furmli, Hossai

AU - Owen, Dylan M.

AU - Savchenko, Alexei

AU - Treanor, Bebhinn

PY - 2018/12/1

Y1 - 2018/12/1

N2 - The galectin family of secreted lectins have emerged as important regulators of immune cell function; however, their role in B-cell responses is poorly understood. Here we identify IgM-BCR as a ligand for galectin-9. Furthermore, we show enhanced BCR microcluster formation and signaling in galectin-9-deficient B cells. Notably, treatment with exogenous recombinant galectin-9 nearly completely abolishes BCR signaling. We investigated the molecular mechanism for galectin-9-mediated inhibition of BCR signaling using super-resolution imaging and single-particle tracking. We show that galectin-9 merges pre-existing nanoclusters of IgM-BCR, immobilizes IgM-BCR, and relocalizes IgM-BCR together with the inhibitory molecules CD45 and CD22. In resting naive cells, we use dual-color super-resolution imaging to demonstrate that galectin-9 mediates the close association of IgM and CD22, and propose that the loss of this association provides a mechanism for enhanced activation of galectin-9-deficient B cells.

AB - The galectin family of secreted lectins have emerged as important regulators of immune cell function; however, their role in B-cell responses is poorly understood. Here we identify IgM-BCR as a ligand for galectin-9. Furthermore, we show enhanced BCR microcluster formation and signaling in galectin-9-deficient B cells. Notably, treatment with exogenous recombinant galectin-9 nearly completely abolishes BCR signaling. We investigated the molecular mechanism for galectin-9-mediated inhibition of BCR signaling using super-resolution imaging and single-particle tracking. We show that galectin-9 merges pre-existing nanoclusters of IgM-BCR, immobilizes IgM-BCR, and relocalizes IgM-BCR together with the inhibitory molecules CD45 and CD22. In resting naive cells, we use dual-color super-resolution imaging to demonstrate that galectin-9 mediates the close association of IgM and CD22, and propose that the loss of this association provides a mechanism for enhanced activation of galectin-9-deficient B cells.

U2 - 10.1038/s41467-018-05771-8

DO - 10.1038/s41467-018-05771-8

M3 - Article

VL - 9

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 3288

ER -