IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v16y2025i1d10.1038_s41467-025-63547-3.html
   My bibliography  Save this article

GM-CSF-dependent CD301b+ mouse lung dendritic cells confer tolerance to inhaled allergens

Author

Listed:
  • Christina L. Wilkinson

    (NIH)

  • Keiko Nakano

    (NIH)

  • Sara A. Grimm

    (NIH)

  • Gregory S. Whitehead

    (NIH)

  • Yukitomo Arao

    (NIH)

  • Perry J. Blackshear

    (NIH)

  • Peer W. Karmaus

    (NIH)

  • Michael B. Fessler

    (NIH)

  • Donald N. Cook

    (NIH)

  • Hideki Nakano

    (NIH)

Abstract

The severity of allergic asthma is driven by the balance between allergen-specific T regulatory (Treg) and T helper (Th)2 cells. However, it is unclear whether specific subsets of conventional dendritic cells (cDCs) promote the differentiation of Tregs. We have identified a subset of lung resident type 2 cDCs (cDC2s) that display high levels of CD301b and have potent Treg-inducing activity ex vivo. Single-cell RNA sequencing and adoptive transfer experiments show that during allergic sensitization, many CD301b+ cDC2s transition in a stepwise manner to CD200+ cDC2s that selectively promote Th2 differentiation. GM-CSF augments the development and maintenance of CD301b+ cDC2s in vivo, and also selectively expands Treg-inducing CD301b+ cDC2s derived from bone marrow. Upon their adoptive transfer to recipient mice, lung-derived CD301b+ cDC2s confer immunological tolerance to inhaled allergens. Thus, GM-CSF maintains lung homeostasis by increasing numbers of Treg-inducing CD301b+ cDC2s.

Suggested Citation

  • Christina L. Wilkinson & Keiko Nakano & Sara A. Grimm & Gregory S. Whitehead & Yukitomo Arao & Perry J. Blackshear & Peer W. Karmaus & Michael B. Fessler & Donald N. Cook & Hideki Nakano, 2025. "GM-CSF-dependent CD301b+ mouse lung dendritic cells confer tolerance to inhaled allergens," Nature Communications, Nature, vol. 16(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-63547-3
    DOI: 10.1038/s41467-025-63547-3
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-025-63547-3
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-025-63547-3?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
    ---><---

    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:16:y:2025:i:1:d:10.1038_s41467-025-63547-3. 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.