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Leukemia inhibitory factor inhibits plasmacytoid dendritic cell function and development

Journal of Immunology, ISSN: 1550-6606, Vol: 204, Issue: 8, Page: 2257-2268
2020
  • 12
    Citations
  • 0
    Usage
  • 16
    Captures
  • 1
    Mentions
  • 35
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    12
  • Captures
    16
  • Mentions
    1
    • News Mentions
      1
      • News
        1
  • Social Media
    35
    • Shares, Likes & Comments
      35
      • Facebook
        35

Most Recent News

ILC2-derived LIF licences progress from tissue to systemic immunity

Nature, Published online: 07 August 2024; doi:10.1038/s41586-024-07746-w Disruption of leukaemia inhibitory factor production from group 2 innate lymphoid cells prevents immune cells leaving the lungs to migrate to lymph nodes, leading to plasmacytoid dendritic cells becoming retained in the lungs following viral infection.

Article Description

Plasmacytoid dendritic cells (pDCs) produce abundant type I IFNs (IFN-I) in response to viral nucleic acids. Generation of pDCs from bone marrow dendritic cell (DC) progenitors and their maintenance is driven by the transcription factor E2-2 and inhibited by its repressor Id2. In this study, we find that mouse pDCs selectively express the receptor for LIF that signals through STAT3. Stimulation of pDCs with LIF inhibited IFN-I, TNF, and IL-6 responses to CpG and induced expression of the STAT3 targets SOCS3 and Bcl3, which inhibit IFN-I and NF-kB signaling. Moreover, although STAT3 has been also reported to induce E2-2, LIF paradoxically induced its repressor Id2. A late-stage bone marrow DC progenitor expressed low amounts of LIFR and developed into pDCs less efficiently after being exposed to LIF, consistent with the induction of Id2. Conversely, pDC development and serum IFN-I responses to lymphocytic choriomeningitis virus infection were augmented in newly generated mice lacking LIFR in either CD11c+ or hematopoietic cells. Thus, an LIF-driven STAT3 pathway induces SOCS3, Bcl3, and Id2, which render pDCs and late DC progenitors refractory to physiological stimuli controlling pDC functions and development. This pathway can be potentially exploited to prevent inappropriate secretion of IFN-I in autoimmune diseases or promote IFN-I secretion during viral infections.

Bibliographic Details

Sesti-Costa, Renata; Cervantes-Barragan, Luisa; Swiecki, Melissa K; Fachi, José Luís; Cella, Marina; Gilfillan, Susan; Silva, João Santana; Colonna, Marco

Oxford University Press (OUP)

Medicine; Immunology and Microbiology

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