Gene profiling reveals unknown enhancing and suppressive actions of glucocorticoids on immune cells

By Jérôme Galon, D. Franchimont, N. Hiroi, G. Frey, A. Boettner, M. Ehrhart‐Bornstein, J. O’Shea, George P. Chrousos, S. Bornstein. The FASEB Journal, 2002

609 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/a461dddd36e4875875e7f91c1b150b86bafaef3d

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In Immunology

Citations in the corpus

Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: Consensus statements from an international task force by the American College of Critical Care Medicine (2008, background): “It has been estimated that GCs affect 20% of the genome of mononuclear blood cells (39).”
Familial and acquired hemophagocytic lymphohistiocytosis (2006, background): “Hyperinflammation, caused by hypercytokinemia, can be suppressed successfully by corticosteroids, which are cytotoxic for lymphocytes, inhibit the expression of cytokines and chemokines [31], and also interfere with the production of CD95 ligand and differentiation of dendritic cells [120].”
Immunological aspects of cancer chemotherapy (2008, background): “Glucocorticoids suppress the production of pro-inflammatory cytokines (such as interferon-α (IFNα), IFNβ, interleukin-1α (IL-1α) and IL-1β) and chemokines (such as CXC-chemokine ligand 8 (CXCL8), CC-chemokine ligand 7 (CCL7), CCL8, CCL11, CCL13, CCL17, CCL19 and CCL20) by blood mononuclear cells fro”
The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “Unfortunately, no convincing apoptotic target genes of GR have been reported so far (124, 126, 197, 314, 632), although a number of gene products are blocking GC-induced apoptosis, such as Bcl-2, Bcl-xL, as well as inhibitors of apoptosis (IAPs) (633–636).”
Pharmacokinetics and Pharmacodynamics of Systemically Administered Glucocorticoids (2005, background): “After down-regulated in a cell-type specific way.[133-135] DNA association, the GR/GC homodimer (together”
The Biology of the Glucocorticoid Receptor: New Signaling Mechanisms in Health and Disease (2013, background): “Following glucocorticoid binding, GR induces or represses the transcription of target genes which can comprise up to 10-20% of the human genome (7-9).”
Parallel SUMOylation-dependent pathways mediate gene- and signal-specific transrepression by LXRs and PPARgamma. (2007, background): “…receptor g (PPARg), retinoic acid receptor (RAR), and estrogen receptors (ERs) revealed that each nuclear receptor represses an overlapping, but distinct, pattern of signal-dependent inflammatory gene expression (Galon et al., 2002; Joseph et al., 2003; Ogawa et al., 2005; Welch et al., 2003).”
Neuroinflammation and depression: A review (2020, background): “All of them focus on the genomic effects of GRs and on the induced expression of immune-related genes promoting pro-inflammatory responses (Chinenov & Rogatsky, 2007; Galon et al., 2002).”