Genomic deletion of Bcl6 differentially affects conventional dendritic cell subsets and compromises Tfh/Tfr/Th17 cell responses

Hongkui Xiao, Isabel Ulmert, Luisa Bach, Johanna Huber, Hamsa Narasimhan, Ilia Kurochkin, Yinshui Chang, Signe Holst, Urs Mörbe, Lili Zhang, Andreas Schlitzer, Carlos-Filipe Pereira, Barbara U. Schraml, Dirk Baumjohann () and Katharina Lahl ()
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Hongkui Xiao: Technical University of Denmark (DTU)
Isabel Ulmert: Technical University of Denmark (DTU)
Luisa Bach: University of Bonn
Johanna Huber: LMU Munich
Hamsa Narasimhan: Ludwig-Maximillians-Universität München
Ilia Kurochkin: Lund University
Yinshui Chang: University of Bonn
Signe Holst: Technical University of Denmark (DTU)
Urs Mörbe: Technical University of Denmark (DTU)
Lili Zhang: University of Bonn
Andreas Schlitzer: University of Bonn
Carlos-Filipe Pereira: Lund University
Barbara U. Schraml: Ludwig-Maximillians-Universität München
Dirk Baumjohann: University of Bonn
Katharina Lahl: Technical University of Denmark (DTU)

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract Conventional dendritic cells (cDC) play key roles in immune induction, but what drives their heterogeneity and functional specialization is still ill-defined. Here we show that cDC-specific deletion of the transcriptional repressor Bcl6 in mice alters the phenotype and transcriptome of cDC1 and cDC2, while their lineage identity is preserved. Bcl6-deficient cDC1 are diminished in the periphery but maintain their ability to cross-present antigen to CD8+ T cells, confirming general maintenance of this subset. Surprisingly, the absence of Bcl6 in cDC causes a complete loss of Notch2-dependent cDC2 in the spleen and intestinal lamina propria. DC-targeted Bcl6-deficient mice induced fewer T follicular helper cells despite a profound impact on T follicular regulatory cells in response to immunization and mounted diminished Th17 immunity to Citrobacter rodentium in the colon. Our findings establish Bcl6 as an essential transcription factor for subsets of cDC and add to our understanding of the transcriptional landscape underlying cDC heterogeneity.

Date: 2024
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DOI: 10.1038/s41467-024-46966-6

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