IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v15y2024i1d10.1038_s41467-024-54757-2.html
   My bibliography  Save this article

Rab8a restores diverse innate functions in CD11c+CD11b+ dendritic cells from aged mice

Author

Listed:
  • Sudhakar Singh

    (Indian Institute of Science Education and Research Mohali)

  • Azeez Tehseen

    (Indian Institute of Science Education and Research Mohali)

  • Surbhi Dahiya

    (Indian Institute of Science Education and Research Mohali)

  • Yuviana J. Singh

    (Indian Institute of Science Education and Research Mohali)

  • Roman Sarkar

    (Indian Institute of Science Education and Research Mohali)

  • Sharvan Sehrawat

    (Indian Institute of Science Education and Research Mohali)

Abstract

Age-related alterations of the immune system compromise the host’s ability to respond to pathogens, but how immune aging is regulated is still poorly understood. Here, we identify via transcriptomic analysis of splenic DCs and bone marrow derived dendritic cells (BMDC) of young and aged mice, the small GTPase Rab8a as a regulator of dendritic cell (DC) functions in mice. CD11c+CD11b+ DCs of aged in comparison to young host exhibit a diminished type I IFN response upon viral stimulation and inefficiently present exogenous antigens to CD8+ T cells in vitro and in vivo. Rab8a overexpression, which is accompanied by the upregulation of Rab11, restores the functionality of these aged DCs, whereas knockdown of Rab8a reduces functionality of DCs from young mice. Mechanistically, Rab8a and Rab11 cooperate to induce efficient trafficking of peptide loaded class I MHC molecules from the ER to the cell surface. We propose that targeting Rab8a might serve as a strategy to restore DC functionality in the context of immune aging.

Suggested Citation

  • Sudhakar Singh & Azeez Tehseen & Surbhi Dahiya & Yuviana J. Singh & Roman Sarkar & Sharvan Sehrawat, 2024. "Rab8a restores diverse innate functions in CD11c+CD11b+ dendritic cells from aged mice," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-54757-2
    DOI: 10.1038/s41467-024-54757-2
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-024-54757-2
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-024-54757-2?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
    ---><---

    References listed on IDEAS

    as
    1. Lin Luo & Adam A. Wall & Jeremy C. Yeo & Nicholas D. Condon & Suzanne J. Norwood & Simone Schoenwaelder & Kaiwen W. Chen & Shaun Jackson & Brendan J. Jenkins & Elizabeth L. Hartland & Kate Schroder & , 2014. "Rab8a interacts directly with PI3Kγ to modulate TLR4-driven PI3K and mTOR signalling," Nature Communications, Nature, vol. 5(1), pages 1-13, December.
    Full references (including those not matched with items on IDEAS)

    Most related items

    These are the items that most often cite the same works as this one and are cited by the same works as this one.
    1. Gloria Ursino & Giorgio Ramadori & Anna Höfler & Soline Odouard & Pryscila D. S. Teixeira & Florian Visentin & Christelle Veyrat-Durebex & Giulia Lucibello & Raquel Firnkes & Serena Ricci & Claudia R., 2022. "Hepatic non-parenchymal S100A9-TLR4-mTORC1 axis normalizes diabetic ketogenesis," Nature Communications, Nature, vol. 13(1), pages 1-17, 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:15:y:2024:i:1:d:10.1038_s41467-024-54757-2. 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.

    If CitEc recognized a bibliographic reference but did not link an item in RePEc to it, you can help with 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.