Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans

Leukocytes are coated with glycans that modulate immune function through interactions with lectins. Here, the authors characterize the N-glycan repertoire of human tonsillar B cells. They report that Gal-9 is an intrinsic regulator of B cell activation that may differentially modulate BCR signaling...

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Main Authors: N. Giovannone, J. Liang, A. Antonopoulos, J. Geddes Sweeney, S. L. King, S. M. Pochebit, N. Bhattacharyya, G. S. Lee, A. Dell, H. R. Widlund, S. M. Haslam, C. J. Dimitroff
Format: Article
Language:English
Published: Nature Publishing Group 2018-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-05770-9
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spelling doaj-e80facbfd7b94762a3e41e78b109cc7d2021-05-11T10:12:30ZengNature Publishing GroupNature Communications2041-17232018-08-019111710.1038/s41467-018-05770-9Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycansN. Giovannone0J. Liang1A. Antonopoulos2J. Geddes Sweeney3S. L. King4S. M. Pochebit5N. Bhattacharyya6G. S. Lee7A. Dell8H. R. Widlund9S. M. Haslam10C. J. Dimitroff11Department of Dermatology, Brigham and Women’s HospitalDepartment of Dermatology, Brigham and Women’s HospitalDepartment of Life Sciences, Imperial College LondonDepartment of Dermatology, Brigham and Women’s HospitalDepartment of Dermatology, Brigham and Women’s HospitalHarvard Medical SchoolDepartment of Surgery, Division of Otolaryngology, Brigham and Women’s HospitalDepartment of Otology and Laryngology, Harvard Medical SchoolDepartment of Life Sciences, Imperial College LondonDepartment of Dermatology, Brigham and Women’s HospitalDepartment of Life Sciences, Imperial College LondonDepartment of Dermatology, Brigham and Women’s HospitalLeukocytes are coated with glycans that modulate immune function through interactions with lectins. Here, the authors characterize the N-glycan repertoire of human tonsillar B cells. They report that Gal-9 is an intrinsic regulator of B cell activation that may differentially modulate BCR signaling at steady state and within germinal centers due to expression of I-branched glycans.https://doi.org/10.1038/s41467-018-05770-9
collection DOAJ
language English
format Article
sources DOAJ
author N. Giovannone
J. Liang
A. Antonopoulos
J. Geddes Sweeney
S. L. King
S. M. Pochebit
N. Bhattacharyya
G. S. Lee
A. Dell
H. R. Widlund
S. M. Haslam
C. J. Dimitroff
spellingShingle N. Giovannone
J. Liang
A. Antonopoulos
J. Geddes Sweeney
S. L. King
S. M. Pochebit
N. Bhattacharyya
G. S. Lee
A. Dell
H. R. Widlund
S. M. Haslam
C. J. Dimitroff
Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans
Nature Communications
author_facet N. Giovannone
J. Liang
A. Antonopoulos
J. Geddes Sweeney
S. L. King
S. M. Pochebit
N. Bhattacharyya
G. S. Lee
A. Dell
H. R. Widlund
S. M. Haslam
C. J. Dimitroff
author_sort N. Giovannone
title Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans
title_short Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans
title_full Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans
title_fullStr Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans
title_full_unstemmed Galectin-9 suppresses B cell receptor signaling and is regulated by I-branching of N-glycans
title_sort galectin-9 suppresses b cell receptor signaling and is regulated by i-branching of n-glycans
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2018-08-01
description Leukocytes are coated with glycans that modulate immune function through interactions with lectins. Here, the authors characterize the N-glycan repertoire of human tonsillar B cells. They report that Gal-9 is an intrinsic regulator of B cell activation that may differentially modulate BCR signaling at steady state and within germinal centers due to expression of I-branched glycans.
url https://doi.org/10.1038/s41467-018-05770-9
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