B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism
The immune response relies on the integration of cell-intrinsic processes with cell-extrinsic cues. During infection, B cells vacate the marrow during emergency granulopoiesis but return upon restoration of homeostasis. Here we report a novel glycosylation-mediated crosstalk between marrow B cells a...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
eLife Sciences Publications Ltd
2019-08-01
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| Series: | eLife |
| Subjects: | |
| Online Access: | https://elifesciences.org/articles/47328 |
| _version_ | 1817967831044587520 |
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| author | Eric E Irons Melissa M Lee-Sundlov Yuqi Zhu Sriram Neelamegham Karin M Hoffmeister Joseph TY Lau |
| author_facet | Eric E Irons Melissa M Lee-Sundlov Yuqi Zhu Sriram Neelamegham Karin M Hoffmeister Joseph TY Lau |
| author_sort | Eric E Irons |
| collection | DOAJ |
| description | The immune response relies on the integration of cell-intrinsic processes with cell-extrinsic cues. During infection, B cells vacate the marrow during emergency granulopoiesis but return upon restoration of homeostasis. Here we report a novel glycosylation-mediated crosstalk between marrow B cells and hematopoietic progenitors. Human B cells secrete active ST6GAL1 sialyltransferase that remodels progenitor cell surface glycans to suppress granulopoiesis. In mouse models, ST6GAL1 from B cells alters the sialylation profile of bone marrow populations, and mature IgD+ B cells were enriched in sialylated bone marrow niches. In clinical multiple myeloma, ST6GAL1 abundance in the multiple myeloma cells negatively correlated with neutrophil abundance. These observations highlight not only the ability of medullary B cells to influence blood cell production, but also the disruption to normal granulopoiesis by excessive ST6GAL1 in malignancy. |
| first_indexed | 2024-04-11T09:04:34Z |
| format | Article |
| id | doaj.art-1e601d2c3f0f4d979c9144d091a5a903 |
| institution | Directory Open Access Journal |
| issn | 2050-084X |
| language | English |
| last_indexed | 2024-04-11T09:04:34Z |
| publishDate | 2019-08-01 |
| publisher | eLife Sciences Publications Ltd |
| record_format | Article |
| series | eLife |
| spelling | doaj.art-1e601d2c3f0f4d979c9144d091a5a9032022-12-22T04:32:40ZengeLife Sciences Publications LtdeLife2050-084X2019-08-01810.7554/eLife.47328B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanismEric E Irons0Melissa M Lee-Sundlov1https://orcid.org/0000-0002-8290-8586Yuqi Zhu2Sriram Neelamegham3Karin M Hoffmeister4Joseph TY Lau5https://orcid.org/0000-0002-5128-2664Department of Molecular and Cellular Biology, Roswell Park Comprehensive Cancer Center, Buffalo, United StatesBlood Research Institute Versiti, Milwaukee, United StatesDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, United StatesDepartment of Chemical and Biological Engineering, University at Buffalo, Buffalo, United StatesBlood Research Institute Versiti, Milwaukee, United StatesDepartment of Molecular and Cellular Biology, Roswell Park Comprehensive Cancer Center, Buffalo, United StatesThe immune response relies on the integration of cell-intrinsic processes with cell-extrinsic cues. During infection, B cells vacate the marrow during emergency granulopoiesis but return upon restoration of homeostasis. Here we report a novel glycosylation-mediated crosstalk between marrow B cells and hematopoietic progenitors. Human B cells secrete active ST6GAL1 sialyltransferase that remodels progenitor cell surface glycans to suppress granulopoiesis. In mouse models, ST6GAL1 from B cells alters the sialylation profile of bone marrow populations, and mature IgD+ B cells were enriched in sialylated bone marrow niches. In clinical multiple myeloma, ST6GAL1 abundance in the multiple myeloma cells negatively correlated with neutrophil abundance. These observations highlight not only the ability of medullary B cells to influence blood cell production, but also the disruption to normal granulopoiesis by excessive ST6GAL1 in malignancy.https://elifesciences.org/articles/47328granulopoiesisglycosylationB cellssialyltransferasehematopoietic |
| spellingShingle | Eric E Irons Melissa M Lee-Sundlov Yuqi Zhu Sriram Neelamegham Karin M Hoffmeister Joseph TY Lau B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism eLife granulopoiesis glycosylation B cells sialyltransferase hematopoietic |
| title | B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism |
| title_full | B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism |
| title_fullStr | B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism |
| title_full_unstemmed | B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism |
| title_short | B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism |
| title_sort | b cells suppress medullary granulopoiesis by an extracellular glycosylation dependent mechanism |
| topic | granulopoiesis glycosylation B cells sialyltransferase hematopoietic |
| url | https://elifesciences.org/articles/47328 |
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