Paola Ricciardi-Castagnoli
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Paola Ricciardi-Castagnoli has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
Francesca Zolezzi
Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A(∗)STAR), Singapore 138648, Singapore
2 shared publications- Michael Poidinger
Singapore Immunology Network, A*STAR, Singapore, Singapore
2 shared publications - Teresa Zelante
Department of Medicine and Surgery, University of Perugia, Perugia, Italy
2 shared publications Akhila Balachander
Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Biopolis, Singapore
1 shared publication- Alessandra Mortellaro
San Raffaele Telethon Institute for Gene Therapy (SR-TIGET), IRCCS San Raffaele Scientific Institute, Milan, Italy
1 shared publication - Alicia Yoke Wei Wong
Department of Medicine and Surgery, University of Perugia, 06129 Perugia, Italy
1 shared publication
Latest Publications
- Open Access
- 1 September 2015
- Published by Elsevier in Cell Reports
- Vol. 12 (11) , 1789-1801
CD103+ Dendritic Cells Control Th17 Cell Function in the Lung
- 1 September 2015
- Published by Elsevier in Cell Reports
- Vol. 12 (11) , 1789-1801
Open AccessCD103+ Dendritic Cells Control Th17 Cell Function in the Lung
- Open Access
- 30 December 2014
- Published by Oxford University Press (OUP) in Nucleic Acids Research
- Vol. 43 (2) , 836-847
NFATc2 mediates epigenetic modification of dendritic cell cytokine and chemokine responses to dectin-1 stimulation
The transcription factor NFATc2 regulates dendritic cell (DC) responses to microbial stimulation through the C-type lectin receptor dectin-1. But the genetic targets of NFATc2 and their effects on DC function remain largely unknown. Therefore we used ChIP-seq to conduct genome-wide mapping of NFATc2 target sites in dectin-1-activated DCs. By combining binding-site data with a comprehensive gene expression profile, we found that NFATc2 occupancy regulates the expression of a subset of dectin-1-activated genes. Surprisingly, NFATc2 targeted an extensive range of DC-derived cytokines and chemokines, including regulatory cytokines such as IL2, IL23a and IL12b. Furthermore, we demonstrated that NFATc2 binding is required to induce the histone 3 lysine 4 trimethylation (H3K4me3) epigenetic mark, which is associated with enhanced gene expression. Together, these data show that the transcription factor NFATc2 mediates epigenetic modification of DC cytokine and chemokine genes leading to activation of their expression.
- 30 December 2014
- Published by Oxford University Press (OUP) in Nucleic Acids Research
- Vol. 43 (2) , 836-847
Open AccessNFATc2 mediates epigenetic modification of dendritic cell cytokine and chemokine responses to dectin-1 stimulation
The transcription factor NFATc2 regulates dendritic cell (DC) responses to microbial stimulation through the C-type lectin receptor dectin-1. But the genetic targets of NFATc2 and their effects on DC function remain largely unknown. Therefore we used ChIP-seq to conduct genome-wide mapping of NFATc2 target sites in dectin-1-activated DCs. By combining binding-site data with a comprehensive gene expression profile, we found that NFATc2 occupancy regulates the expression of a subset of dectin-1-activated genes. Surprisingly, NFATc2 targeted an extensive range of DC-derived cytokines and chemokines, including regulatory cytokines such as IL2, IL23a and IL12b. Furthermore, we demonstrated that NFATc2 binding is required to induce the histone 3 lysine 4 trimethylation (H3K4me3) epigenetic mark, which is associated with enhanced gene expression. Together, these data show that the transcription factor NFATc2 mediates epigenetic modification of DC cytokine and chemokine genes leading to activation of their expression.