ReviewThe Journal of biological chemistry2017
Glucocorticoid and cytokine crosstalk: Feedback, feedforward, and co-regulatory interactions determine repression or resistance.
Review in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05078021 (Phenotyping Disease Severity in Asthma), which is not on this map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Phenotyping Disease Severity in Asthma: Molecular Investigations of Corticosteroid
Who cites it
50 citing papers in PubMed, 90 citations in OpenAlex.
- Distinct immunomodulatory effects of synthetic progestins compared with natural progesterone in human immune cells.ImmunoHorizons · 2026Article
- Inter-Organ Communication Networks in Systemic Physiology: Glucocorticoid Receptor α as a Central Integrator of Homeostasis.International journal of molecular sciences · 2026Review
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- The Impact of Stress on the Functioning and Survival of Transplanted Kidneys-Biological Mechanisms, Clinical Implications, and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- Differential RELA and GR recruitment to the BIRC3/BIRC2 locus: Molecular insight as to combinatorial regulation by proinflammatory cytokines and glucocorticoid.Molecular pharmacology · 2025Article
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- Gut Microbiota-Derived Butyric Acid Alleviates Glucocorticoid-Associated Osteonecrosis of the Femoral Head via Modulating Inflammatory Cytokines in Bone Marrow Mesenchymal Stem Cells.Mediators of inflammation · 2025Article
- A20 in Kidney Transplantation and Autoimmunity.International journal of molecular sciences · 2024Review
- Complement C5a Receptor Signaling Alters Stress Responsiveness and Modulates Microglia Following Chronic Stress Exposure.Biological psychiatry global open science · 2024Article
- Comparative safety, pharmacokinetics, and off-target assessment of 1,1-bis(3'-indolyl)-1-(Toxicology research · 2024Article
- Glucocorticoid receptor-dependent therapeutic efficacy of tauroursodeoxycholic acid in preclinical models of spinocerebellar ataxia type 3.The Journal of clinical investigation · 2024Article
- Endothelial Jagged1 levels and distribution are post-transcriptionally controlled by ZFP36 decay proteins.Cell reports · 2024Article
- Global analysis of the abundance of AU-rich mRNAs in response to glucocorticoid treatment.Scientific reports · 2024Article
- Chronic Stress as a Risk Factor for Type 2 Diabetes: Endocrine, Metabolic, and Immune Implications.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Enrichment of a neutrophil-like monocyte transcriptional state in glioblastoma myeloid suppressor cells.Research square · 2023Article
- Article
- Bronchial epithelial cell transcriptional responses to inhaled corticosteroids dictate severe asthmatic outcomes.The Journal of allergy and clinical immunology · 2023Article
- Glucocorticoids and medroxyprogesterone acetate synergize with inflammatory stimuli to selectively upregulate CCL20 transcription.Molecular and cellular endocrinology · 2023Article
- Phase-separation: a possible new layer for transcriptional regulation by glucocorticoid receptor.Frontiers in endocrinology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 4 countries.
Funding
Abstract
Inflammatory signals induce feedback and feedforward systems that provide temporal control. Although glucocorticoids can repress inflammatory gene expression, glucocorticoid receptor recruitment increases expression of negative feedback and feedforward regulators, including the phosphatase, DUSP1, the ubiquitin-modifying enzyme, TNFAIP3, or the mRNA-destabilizing protein, ZFP36. Moreover, glucocorticoid receptor cooperativity with factors, including nuclear factor-κB (NF-κB), may enhance regulator expression to promote repression. Conversely, MAPKs, which are inhibited by glucocorticoids, provide feedforward control to limit expression of the transcription factor IRF1, and the chemokine, CXCL10. We propose that modulation of feedback and feedforward control can determine repression or resistance of inflammatory gene expression toglucocorticoid.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.