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Compensatory dendritic cell development mediated by BATF–IRF interactions

Author

Listed:
  • Roxane Tussiwand

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Wan-Ling Lee

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Theresa L. Murphy

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Mona Mashayekhi

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Wumesh KC

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Jörn C. Albring

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Ansuman T. Satpathy

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Jeffrey A. Rotondo

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Brian T. Edelson

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Nicole M. Kretzer

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Xiaodi Wu

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Leslie A. Weiss

    (Washington University School of Medicine)

  • Elke Glasmacher

    (Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA)

  • Peng Li

    (Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Wei Liao

    (Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Michael Behnke

    (Washington University School of Medicine)

  • Samuel S. K. Lam

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Cora T. Aurthur

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Warren J. Leonard

    (Laboratory of Molecular Immunology and Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Harinder Singh

    (Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA)

  • Christina L. Stallings

    (Washington University School of Medicine)

  • L. David Sibley

    (Washington University School of Medicine)

  • Robert D. Schreiber

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

  • Kenneth M. Murphy

    (Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA
    Howard Hughes Medical Institute, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA)

Abstract

The AP1 transcription factor Batf3 is required for homeostatic development of CD8α+ classical dendritic cells that prime CD8 T-cell responses against intracellular pathogens. Here we identify an alternative, Batf3-independent pathway in mice for CD8α+ dendritic cell development operating during infection with intracellular pathogens and mediated by the cytokines interleukin (IL)-12 and interferon-γ. This alternative pathway results from molecular compensation for Batf3 provided by the related AP1 factors Batf, which also functions in T and B cells, and Batf2 induced by cytokines in response to infection. Reciprocally, physiological compensation between Batf and Batf3 also occurs in T cells for expression of IL-10 and CTLA4. Compensation among BATF factors is based on the shared capacity of their leucine zipper domains to interact with non-AP1 factors such as IRF4 and IRF8 to mediate cooperative gene activation. Conceivably, manipulating this alternative pathway of dendritic cell development could be of value in augmenting immune responses to vaccines.

Suggested Citation

  • Roxane Tussiwand & Wan-Ling Lee & Theresa L. Murphy & Mona Mashayekhi & Wumesh KC & Jörn C. Albring & Ansuman T. Satpathy & Jeffrey A. Rotondo & Brian T. Edelson & Nicole M. Kretzer & Xiaodi Wu & Lesl, 2012. "Compensatory dendritic cell development mediated by BATF–IRF interactions," Nature, Nature, vol. 490(7421), pages 502-507, October.
    • Handle: RePEc:nat:nature:v:490:y:2012:i:7421:d:10.1038_nature11531
    DOI: 10.1038/nature11531
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    Cited by:

    1. Nikolai Schleussner & Pierre Cauchy & Vedran Franke & Maciej Giefing & Oriol Fornes & Naveen Vankadari & Salam A. Assi & Mariantonia Costanza & Marc A. Weniger & Altuna Akalin & Ioannis Anagnostopoulo, 2023. "Transcriptional reprogramming by mutated IRF4 in lymphoma," Nature Communications, Nature, vol. 14(1), pages 1-18, December.
    2. Yali Liu & Meng Qu & Han Jiang & Ralf Schneider & Geng Qin & Wei Luo & Haiyan Yu & Bo Zhang & Xin Wang & Yanhong Zhang & Huixian Zhang & Zhixin Zhang & Yongli Wu & Yingyi Zhang & Jianping Yin & Si Zha, 2022. "Immunogenetic losses co-occurred with seahorse male pregnancy and mutation in tlx1 accompanied functional asplenia," Nature Communications, Nature, vol. 13(1), pages 1-12, December.

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