Klf4 expression in conventional dendritic cells is required for T helper 2 cell responses

Tussiwand, Roxane and Everts, Bart and Grajales-Reyes, Gary E. and Kretzer, Nicole M. and Iwata, Arifumi and Bagaitkar, Juhi and Wu, Xiaodi and Wong, Rachel and Anderson, David A. and Murphy, Theresa L. and Pearce, Edward J. and Murphy, Kenneth M.. (2015) Klf4 expression in conventional dendritic cells is required for T helper 2 cell responses. Immunity, 42 (5). pp. 916-928.

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Official URL: https://edoc.unibas.ch/62509/

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The two major lineages of classical dendritic cells (cDCs) express and require either IRF8 or IRF4 transcription factors for their development and function. IRF8-dependent cDCs promote anti-viral and T-helper 1 (Th1) cell responses, whereas IRF4-expressing cDCs have been implicated in controlling both Th2 and Th17 cell responses. Here, we have provided evidence that Kruppel-like factor 4 (Klf4) is required in IRF4-expressing cDCs to promote Th2, but not Th17, cell responses in vivo. Conditional Klf4 deletion within cDCs impaired Th2 cell responses during Schistosoma mansoni infection, Schistosoma egg antigen (SEA) immunization, and house dust mite (HDM) challenge without affecting cytotoxic T lymphocyte (CTL), Th1 cell, or Th17 cell responses to herpes simplex virus, Toxoplasma gondii, and Citrobacter rodentium infections. Further, Klf4 deletion reduced IRF4 expression in pre-cDCs and resulted in selective loss of IRF4-expressing cDCs subsets in several tissues. These results indicate that Klf4 guides a transcriptional program promoting IRF4-expressing cDCs heterogeneity.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Immune Regulation (Tussiwand)
UniBasel Contributors:Tussiwand, Roxane
Item Type:Article, refereed
Article Subtype:Research Article
ISSN:1097-4180 (Electronic) 1074-7613 (Linking)
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:01 Dec 2018 14:45
Deposited On:01 Dec 2018 14:45

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