Cited by 408Estrogen and related hormone effectsT-cell and B-cell ImmunologyAdrenal Hormones and Disorders

Overview of the actions of glucocorticoids on the immune response: a good model to characterize new pathways of immunosuppression for new treatment strategies

FRANCHIMONT, D·2004·Annals of the New York Academy of Sciences

Abstract

A bstract : Glucocorticoids have been used for over 50 years in the treatment of inflammatory and autoimmune diseases and in preventing graft rejection. Today, knowledge of their molecular, cellular, and pharmacological properties allows a better understanding of glucocorticoid‐mediated immunosuppression. Glucocorticoids exert both negative and positive effects with a dynamic and bi‐directional spectrum of activities on various limbs and components of the immune response. They modulate genes involved in the priming of the innate immune response, while their actions on the adaptive immune response are to suppress cellular (Th1) immunity and promote humoral (Th2) immunity. Interestingly, glucocorticoids can also induce tolerance to specific antigens by influencing dendritic cell maturation and function and promoting the development of regulatory high IL‐10‐producing T cells. The ex vivo therapeutic use of glucocorticoids could therefore represent an adjuvant treatment to cell therapy in autoimmune diseases, avoiding the long‐term deleterious adverse effects of glucocorticoids. Thus, the panoramic view of glucocorticoid actions on the immune system provides an interesting model for characterizing important biological pathways of immunosuppression.

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Crossref · 10.1196/annals.1321.009

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  • Glucocorticoids regulate dendritic cell maturation, survival, and motility and hamper their immunogenic functions, including restricting T cell stimulation by preventing up-regulation of MHCII, B7.2, and CD40.

    “In addition to regulating the maturation, survival, and motility of these antigen-presenting cells, GCs also hamper their immunogenic functions. Indeed, the end product of the HPA axis restricts the capacity of DCs to stimulate T cells by preventing the up-regulation of various co-stimulatory molecules, such as MHCII, B7.2 (CD86), and CD40 (33, 36, 37).”

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Authors
FRANCHIMONT, D.
Affiliations
Université Libre de Bruxelles (BE)
Corresponding author
FRANCHIMONT, D
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2004-06
Volume
1024
Issue
1
Pages
124-137
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W2074432289
Cited by
408
References
87
Citations by year
2026: 14 · 2025: 14 · 2024: 10 · 2023: 11 · 2022: 15 · 2021: 16 · 2020: 15 · 2019: 15 · 2018: 20 · 2017: 24 · 2016: 21 · 2015: 24 · 2014: 21 · 2013: 22 · 2012: 26
FWCI
2.39
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
glucocorticoids, immunosuppression, immune response, Th1/Th2 balance, innate immunity, adaptive immunity, dendritic cell maturation, regulatory T cells, IL-10, antigen tolerance, autoimmune disease, graft rejection, glucocorticoid adverse effects
MeSH terms
Animals, Antibody Formation, Glucocorticoids, Humans, Hypersensitivity, Immediate, Immune Tolerance, Immunity, Cellular, Immunity, Innate, Immunosuppressive Agents, Inflammation, T-Lymphocytes, Antigen Presentation, Models, Immunological

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