Glucocorticoids (GCs) have important immunoregulatory effects on thymocytes and T cells. Ectopic production of GCs has been demonstrated in thymic epithelial cells (TECs) but the role of GCs in thymocyte homeostasis is controversial. Studies in several different mouse models, genetically modified for the GC receptor (GR) expression or function, have demonstrated conflicting results in terms of the effect of the hormone on thymocytes. Here, we summarize these data and suggest that GCs can mediate both positive and negative effects in the organ depending on the local hormonal concentration. Basal GC levels might promote growth of early thymocytes in young mice, and increased levels, generated through a stress reaction, apoptosis in these cells. A gradual loss of GC synthesis in TECs during aging might contribute to thymic involution, a process so far unexplained.
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http://dx.doi.org/10.1016/j.it.2004.09.003 | DOI Listing |
Rev Gastroenterol Peru
January 2025
Servicio de Gastroenterología, Hospital Clínico de la Universidad de Chile, Universidad de Chile, Santiago, Chile.
Introduction: Despite advancements in therapeutic strategies, corticosteroids continue to play a role in inducing remission in Inflammatory Bowel Disease (IBD). Unfortunately, these drugs are often misused.
Objectives: To assess the dose and duration of corticosteroid therapy,and the subsequent change in treatment among patients with IBD.
Int Immunopharmacol
January 2025
Laboratório de Citocinas Dept. of Immunology Instituto de Microbiologia Prof. Paulo de Góes Universidade Federal do Rio de Janeiro Rio de Janeiro Brazil.
Introduction: The spectrum of eosinophil functions has expanded from fighting helminths to multiple novel roles in malignancy, infection, cancer, and metabolism. In asthma, glucocorticoids, prostaglandins (PG), and cysteinyl-leukotrienes (LT) regulate eosinophil biology through separate signaling pathways. Here we've evaluated the complex interplay between Dexa, PGE2, and CysLTs in eosinopoiesis and eosinophil biology in an allergic asthma model.
View Article and Find Full Text PDFCurr Treatm Opt Rheumatol
December 2024
Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA USA.
Purpose Of Review: To summarize the current treatment landscape of rheumatoid arthritis-associated interstitial lung disease (RA-ILD) in the context of the recent 2023 American College of Rheumatology/American College of Chest Physicians guideline for ILD treatment in systemic autoimmune rheumatic diseases.
Recent Findings: The guideline conditionally recommends mycophenolate, azathioprine, and rituximab for first-line RA-ILD therapy, with cyclophosphamide and short-term glucocorticoids as additional options. For RA-ILD progression after first line, mycophenolate, rituximab, nintedanib, tocilizumab, cyclophosphamide, and pirfenidone are conditionally recommended, while long-term glucocorticoids are conditionally recommended against.
Inflamm Res
January 2025
Institute of Otolaryngology head and neck surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Objective: This study seeks to elucidate the role and molecular mechanisms of IL-8 in nasal epithelial cell pyroptosis and its impact on glucocorticoid (GC) resistance.
Methods: We assessed the expression of pyroptosis-related biomarkers and IL-8 in tissues and human nasal epithelial cells (hNECs) from both control and nasal polyp patients using western blot. Their localization was determined through immunohistochemistry and immunofluorescence.
Endocrinology
January 2025
Anne M. Delany, PhD, Center for Molecular Oncology, UConn Health, Farmington, CT.
Glucocorticoid excess causes bone loss due to decreased bone formation and increased bone resorption; miR-433-3p is a miRNA that negatively regulates bone formation in male mice by targeting Runx2 as well as RNAs involved in Wnt, protein kinase A and endogenous glucocorticoid signaling. To examine the impact of miR-433-3p on glucocorticoid-mediated bone loss, transgenic mice expressing a miR-433-3p tough decoy inhibitor in the osteoblast lineage were administered prednisolone via slow-release pellets. Bone loss was greater in control mice treated with prednisolone compared with miR-433-3p tough decoy mice due to higher osteoclast activity in the controls.
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