Compensatory dendritic cell development mediated by BATF–IRF interactions

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, Leslie A. Weiss, Elke Glasmacher, Peng Li, Wei Liao, Michael Behnke, Samuel S. K. Lam, Cora T. Aurthur, Warren J. Leonard, Harinder Singh, Christina L. Stallings, L. David Sibley, Robert D. Schreiber and Kenneth M. Murphy ()
Additional contact information
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

Nature, 2012, vol. 490, issue 7421, 502-507

Abstract: 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.

Date: 2012
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DOI: 10.1038/nature11531

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