Compensatory dendritic cell development mediated by BATF-IRF interactions
The AP-1 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 for their development operating during infection with intracellu...
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2012
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482832/ |
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pubmed-34828322013-04-25 Compensatory dendritic cell development mediated by BATF-IRF interactions Tussiwand, Roxane Lee, Wan-Ling Murphy, Theresa L. Mashayekhi, Mona Wumesh, KC Albring, Jörn C. Satpathy, Ansuman T. Rotondo, Jeffrey A. Edelson, Brian T. Kretzer, Nicole M. Wu, Xiaodi Weiss, Leslie A. Glasmacher, Elke Li, Peng Liao, Wei Behnke, Michael Lam, Samuel S.K. Aurthur, Cora T. Leonard, Warren J. Singh, Harinder Stallings, Christina L. Sibley, L. David Schreiber, Robert D. Murphy, Kenneth M. Article The AP-1 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 for their development operating during infection with intracellular pathogens mediated by the cytokines IL-12 and IFN-γ. This alternative pathway results from molecular compensation for Batf3 provided by the related AP-1 factors Batf, which also functions in T and B cells, and Batf2 induced by cytokines in response to infection. Reciprocally, physiologic compensation between Batf and Batf3 also occurs in T cells for expression of IL-10 and CTLA-4. Compensation among BATF factors is based on the shared capacity of their leucine zipper domains to interact with non-AP-1 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. 2012-09-19 2012-10-25 /pmc/articles/PMC3482832/ /pubmed/22992524 http://dx.doi.org/10.1038/nature11531 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms |
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Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
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NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Tussiwand, Roxane Lee, Wan-Ling Murphy, Theresa L. Mashayekhi, Mona Wumesh, KC Albring, Jörn C. Satpathy, Ansuman T. Rotondo, Jeffrey A. Edelson, Brian T. Kretzer, Nicole M. Wu, Xiaodi Weiss, Leslie A. Glasmacher, Elke Li, Peng Liao, Wei Behnke, Michael Lam, Samuel S.K. Aurthur, Cora T. Leonard, Warren J. Singh, Harinder Stallings, Christina L. Sibley, L. David Schreiber, Robert D. Murphy, Kenneth M. |
| spellingShingle |
Tussiwand, Roxane Lee, Wan-Ling Murphy, Theresa L. Mashayekhi, Mona Wumesh, KC Albring, Jörn C. Satpathy, Ansuman T. Rotondo, Jeffrey A. Edelson, Brian T. Kretzer, Nicole M. Wu, Xiaodi Weiss, Leslie A. Glasmacher, Elke Li, Peng Liao, Wei Behnke, Michael Lam, Samuel S.K. Aurthur, Cora T. Leonard, Warren J. Singh, Harinder Stallings, Christina L. Sibley, L. David Schreiber, Robert D. Murphy, Kenneth M. Compensatory dendritic cell development mediated by BATF-IRF interactions |
| author_facet |
Tussiwand, Roxane Lee, Wan-Ling Murphy, Theresa L. Mashayekhi, Mona Wumesh, KC Albring, Jörn C. Satpathy, Ansuman T. Rotondo, Jeffrey A. Edelson, Brian T. Kretzer, Nicole M. Wu, Xiaodi Weiss, Leslie A. Glasmacher, Elke Li, Peng Liao, Wei Behnke, Michael Lam, Samuel S.K. Aurthur, Cora T. Leonard, Warren J. Singh, Harinder Stallings, Christina L. Sibley, L. David Schreiber, Robert D. Murphy, Kenneth M. |
| author_sort |
Tussiwand, Roxane |
| title |
Compensatory dendritic cell development mediated by BATF-IRF interactions |
| title_short |
Compensatory dendritic cell development mediated by BATF-IRF interactions |
| title_full |
Compensatory dendritic cell development mediated by BATF-IRF interactions |
| title_fullStr |
Compensatory dendritic cell development mediated by BATF-IRF interactions |
| title_full_unstemmed |
Compensatory dendritic cell development mediated by BATF-IRF interactions |
| title_sort |
compensatory dendritic cell development mediated by batf-irf interactions |
| description |
The AP-1 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 for their development operating during infection with intracellular pathogens mediated by the cytokines IL-12 and IFN-γ. This alternative pathway results from molecular compensation for Batf3 provided by the related AP-1 factors Batf, which also functions in T and B cells, and Batf2 induced by cytokines in response to infection. Reciprocally, physiologic compensation between Batf and Batf3 also occurs in T cells for expression of IL-10 and CTLA-4. Compensation among BATF factors is based on the shared capacity of their leucine zipper domains to interact with non-AP-1 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. |
| publishDate |
2012 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482832/ |
| _version_ |
1611919454428463104 |