Minireview: glucocorticoids in autoimmunity: unexpected targets and mechanisms

Flammer, Jamie R.; Rogatsky, Inez

doi:10.1210/me.2011-0068

Cited by 140Estrogen and related hormone effectsAdrenal Hormones and DisordersStress Responses and Cortisol

Minireview: glucocorticoids in autoimmunity: unexpected targets and mechanisms

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Flammer, Jamie R., Rogatsky, Inez·2011·Molecular Endocrinology

DOI 10.1210/me.2011-0068PMC PMC5417249

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Abstract

For decades, natural and synthetic glucocorticoids (GC) have been among the most commonly prescribed classes of immunomodulatory drugs. Their unsurpassed immunosuppressive and antiinflammatory activity along with cost-effectiveness makes these compounds a treatment of choice for the majority of autoimmune and inflammatory diseases, despite serious side effects that frequently accompany GC therapy. The activated GC receptor (GR) that conveys the signaling information of these steroid ligands to the transcriptional machinery engages a number of pathways to ultimately suppress autoimmune responses. Of those, GR-mediated apoptosis of numerous cell types of hematopoietic origin and suppression of proinflammatory cytokine gene expression have been described as the primary mechanisms responsible for the antiinflammatory actions of GC. However, along with the ever-increasing appreciation of the complex functions of the immune system in health and disease, we are beginning to recognize new facets of GR actions in immune cells. Here, we give a brief overview of the extensive literature on the antiinflammatory activities of GC and discuss in greater detail the unexpected pathways, factors, and mechanisms that have recently begun to emerge as novel targets for GC-mediated immunosuppression.

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Liganded GRs impact gene transcription through non-genomic mechanisms that do not require de novo protein synthesis and underlie the more rapid actions of GCs.
“In addition to their genomic actions, liganded GRs also impact on gene transcription through various non-genomic mechanisms. These mechanisms do not require de novo protein synthesis and thus underlie the more rapid actions of GCs.”
From The HPA â€“ Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [93]
Prominent non-genomic examples include mRNA destabilization, competition for co-activators, and interference with the binding of transcription factors to DNA.
“Prominent examples include mRNA destabilization, competition for co-activators [e.g., CREB-binding protein (CBP), p300, and GRIP], and interference with the binding of transcription factors to DNA (91–94).”
From The HPA â€“ Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [93]

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“Indeed, GC were shown to inhibit the activity of TANK-binding kinase (TBK)1 that activates IRF3 and IRF7, key components of the IFN enhanceosome (101, 105).”
Background
IRF4 and its regulators: evolving insights into the pathogenesis of inflammatory arthritis?
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Induction of autoantibodies to the adrenal cortex and pancreatic islet cells by interferon alpha therapy for chronic hepatitis C
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The Genomic Analysis of the Impact of Steroid Receptor Coactivators Ablation on Hepatic Metabolism
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Farrerol Ameliorates TNBS-Induced Colonic Inflammation by Inhibiting ERK1/2, JNK1/2, and NF-κB Signaling Pathway
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Glucocorticosteroids in Nano-Sterically Stabilized Liposomes Are Efficacious for Elimination of the Acute Symptoms of Experimental Cerebral Malaria
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Allergic and Immunologic Perspectives of Inflammatory Bowel Disease
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Authors: Flammer, J. R., & Rogatsky, I.
Affiliations: Hospital for Special Surgery (US)
ORCID: Rogatsky, Inez
Venue: Molecular Endocrinology
Publisher: The Endocrine Society
Published: 2011-07-01
Volume: 25
Issue: 7
Pages: 1075-1086
ISSN: 0888-8809 (ISSN-L)
1944-9917
DOI: 10.1210/me.2011-0068
PMC: PMC5417249
OpenAlex: W2021846928
Cited by: 140
References: 131
Citations by year: 2026: 5 · 2025: 8 · 2024: 6 · 2023: 6 · 2022: 6 · 2021: 10 · 2020: 3 · 2019: 9 · 2018: 11 · 2017: 8 · 2016: 6 · 2015: 10 · 2014: 22 · 2013: 10 · 2012: 15
FWCI: 1.68
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Molecular Endocrinology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords: glucocorticoids, glucocorticoid receptor, autoimmunity, immunosuppression, anti-inflammatory mechanism, apoptosis, inflammatory cytokines, hematopoietic cells, novel therapeutic targets, glucocorticoid adverse effects
MeSH terms: Animals, Glucocorticoids, T-Lymphocytes, Helper-Inducer, Humans, Interferon Type I, Lymphocyte Activation, Receptors, Glucocorticoid, Signal Transduction, Autoimmunity, STAT Transcription Factors

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Minireview: glucocorticoids in autoimmunity: unexpected targets and mechanisms

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