IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v12y2021i1d10.1038_s41467-021-22230-z.html
   My bibliography  Save this article

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

Author

Listed:
  • 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
    Ben-Gurion University of the Negev)

  • Claudia Mauri

    (University College London)

  • Idit Shachar

    (The Weizmann Institute of Science)

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.

Suggested Citation

  • 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 & , 2021. "The survival and function of IL-10-producing regulatory B cells are negatively controlled by SLAMF5," Nature Communications, Nature, vol. 12(1), pages 1-14, December.
  • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22230-z
    DOI: 10.1038/s41467-021-22230-z
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-021-22230-z
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-021-22230-z?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Sophie Hillion & Anjelica Miranda & Christelle Dantec & Marina Boudigou & Laƫtitia Pottier & Divi Cornec & Raul M. Torres & Roberta Pelanda, 2024. "Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    2. Juan F. Quintana & Praveena Chandrasegaran & Matthew C. Sinton & Emma M. Briggs & Thomas D. Otto & Rhiannon Heslop & Calum Bentley-Abbot & Colin Loney & Luis de Lecea & Neil A. Mabbott & Annette MacLe, 2022. "Single cell and spatial transcriptomic analyses reveal microglia-plasma cell crosstalk in the brain during Trypanosoma brucei infection," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22230-z. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.