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International Journal of Clinical and Experimental Pathology|February 20, 2014
NOX1 is responsible for cell death through STAT3 activation in hyperoxia and is associated with the pathogenesis of acute respiratory distress syndromeStephanie Carnesecchi, Isabelle Dunand-Sauthier, Filippo Zanetti, et al.
Plos One|February 4, 2014
Interferon-γ induces expression of MHC class II on intestinal epithelial cells and protects mice from colitisChristoph Thelemann, Remzi Onur Eren, Manuel Coutaz, et al.
Life Science Alliance|December 26, 2018
Absence of MHC-II expression by lymph node stromal cells results in autoimmunityJuan Dubrot, Fernanda V Duraes, Guillaume Harlé, et al.
Nature Communications|December 1, 2023
Intrinsic factors and CD1d1 but not CD1d2 expression levels control invariant natural killer T cell subset differentiationLudivine Amable, Luis Antonio Ferreira Martins, Remi Pierre, et al.
Nucleic Acids Research|August 9, 2014
Extensive remodeling of DC function by rapid maturation-induced transcriptional silencingQueralt Seguín-Estévez, Isabelle Dunand-Sauthier, Sylvain Lemeille, et al.
Journal of Immunology (Baltimore, Md. : 1950)|August 13, 2014
Hepatocyte growth factor limits autoimmune neuroinflammation via glucocorticoid-induced leucine zipper expression in dendritic cellsMahdia Benkhoucha, Nicolas Molnarfi, Isabelle Dunand-Sauthier, et al.
Journal of Immunology (Baltimore, Md. : 1950)|June 24, 2015
TLR3-Mediated CD8+ Dendritic Cell Activation Is Coupled with Establishment of a Cell-Intrinsic Antiviral StateLajos Széles, Felix Meissner, Isabelle Dunand-Sauthier, et al.
Proceedings of the National Academy of Sciences of the United States of America|September 20, 2006
Functional CD8+ but not CD4+ T cell responses develop independent of thymic epithelial MHCMarianne M Martinic, Maries F van den Broek, Thomas Rülicke, et al.
The Journal of Experimental Medicine|April 23, 2014
Leucine-rich repeat containing 8A (LRRC8A) is essential for T lymphocyte development and functionLalit Kumar, Janet Chou, Christina S K Yee, et al.
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