The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5
Regulatory B (Breg) cells suppress excessive inflammation primary via the production of interleukin 10 (IL-10). Here the authors show that the function and homeostasis of mouse and human IL-10+ Breg cells are negatively regulated by the cell surface receptor, SLAMF5, to impact experimental autoimmun...
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2021-03-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-021-22230-z |
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doaj-9e0225d58b0f4b71aa42bed1e5fd6e182021-03-28T11:11:35ZengNature Publishing GroupNature Communications2041-17232021-03-0112111410.1038/s41467-021-22230-zThe survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5Lihi Radomir0Matthias P. Kramer1Michal Perpinial2Nofar Schottlender3Stav Rabani4Keren David5Anna Wiener6Hadas Lewinsky7Shirly Becker-Herman8Rina Aharoni9Ron Milo10Claudia Mauri11Idit Shachar12Department of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Immunology, The Weizmann Institute of ScienceDepartment of Neurology, Barzilai University Medical CenterCentre for Rheumatology Research, Department of Medicine, University College LondonDepartment of Immunology, The Weizmann Institute of ScienceRegulatory B (Breg) cells suppress excessive inflammation primary via the production of interleukin 10 (IL-10). Here the authors show that the function and homeostasis of mouse and human IL-10+ Breg cells are negatively regulated by the cell surface receptor, SLAMF5, to impact experimental autoimmunity, thereby hinting SLAMF5 as a potential target for immunotherapy.https://doi.org/10.1038/s41467-021-22230-z |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lihi Radomir Matthias P. Kramer Michal Perpinial Nofar Schottlender Stav Rabani Keren David Anna Wiener Hadas Lewinsky Shirly Becker-Herman Rina Aharoni Ron Milo Claudia Mauri Idit Shachar |
spellingShingle |
Lihi Radomir Matthias P. Kramer Michal Perpinial Nofar Schottlender Stav Rabani Keren David Anna Wiener Hadas Lewinsky Shirly Becker-Herman Rina Aharoni Ron Milo Claudia Mauri Idit Shachar The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 Nature Communications |
author_facet |
Lihi Radomir Matthias P. Kramer Michal Perpinial Nofar Schottlender Stav Rabani Keren David Anna Wiener Hadas Lewinsky Shirly Becker-Herman Rina Aharoni Ron Milo Claudia Mauri Idit Shachar |
author_sort |
Lihi Radomir |
title |
The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 |
title_short |
The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 |
title_full |
The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 |
title_fullStr |
The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 |
title_full_unstemmed |
The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5 |
title_sort |
survival and function of il-10-producing regulatory b cells are negatively controlled by slamf5 |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2021-03-01 |
description |
Regulatory B (Breg) cells suppress excessive inflammation primary via the production of interleukin 10 (IL-10). Here the authors show that the function and homeostasis of mouse and human IL-10+ Breg cells are negatively regulated by the cell surface receptor, SLAMF5, to impact experimental autoimmunity, thereby hinting SLAMF5 as a potential target for immunotherapy. |
url |
https://doi.org/10.1038/s41467-021-22230-z |
work_keys_str_mv |
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