The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5

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 and Idit Shachar ()
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Lihi Radomir: The Weizmann Institute of Science
Matthias P. Kramer: The Weizmann Institute of Science
Michal Perpinial: The Weizmann Institute of Science
Nofar Schottlender: The Weizmann Institute of Science
Stav Rabani: The Weizmann Institute of Science
Keren David: The Weizmann Institute of Science
Anna Wiener: The Weizmann Institute of Science
Hadas Lewinsky: The Weizmann Institute of Science
Shirly Becker-Herman: The Weizmann Institute of Science
Rina Aharoni: The Weizmann Institute of Science
Ron Milo: Barzilai University Medical Center
Claudia Mauri: University College London
Idit Shachar: The Weizmann Institute of Science

Nature Communications, 2021, vol. 12, issue 1, 1-14

Abstract: Abstract B cells have essential functions in multiple sclerosis and in its mouse model, experimental autoimmune encephalomyelitis, both as drivers and suppressors of the disease. The suppressive effects are driven by a regulatory B cell (Breg) population that functions, primarily but not exclusively, via the production of IL-10. However, the mechanisms modulating IL-10-producing Breg abundance are poorly understood. Here we identify SLAMF5 for controlling IL-10+ Breg maintenance and function. In EAE, the deficiency of SLAMF5 in B cells causes accumulation of IL10+ Bregs in the central nervous system and periphery. Blocking SLAMF5 in vitro induces both human and mouse IL-10-producing Breg cells and increases their survival with a concomitant increase of a transcription factor, c-Maf. Finally, in vivo SLAMF5 blocking in EAE elevates IL-10+ Breg levels and ameliorates disease severity. Our results suggest that SLAMF5 is a negative moderator of IL-10+ Breg cells, and may serve as a therapeutic target in MS and other autoimmune diseases.

Date: 2021
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DOI: 10.1038/s41467-021-22230-z

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