Related Experiment Video
Updated: Mar 22, 2026
07:37
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
1.4K
Reduced corticosteroid-binding globulin cleavage in active rheumatoid arthritis
Marni A Nenke1,2, John G Lewis3, Wayne Rankin1,2,4
1Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA, Australia.
Clinical Endocrinology
|April 11, 2016
Summary
Patients with rheumatoid arthritis (RA) show reduced corticosteroid-binding globulin (CBG) cleavage, impairing cortisol delivery to inflamed joints. This impaired CBG function may contribute to chronic inflammation in RA.
Area of Science:
- Endocrinology
- Immunology
- Rheumatology
Background:
- Corticosteroid-binding globulin (CBG) transports cortisol, releasing bioavailable cortisol at inflammation sites.
- Rheumatoid arthritis (RA) is responsive to glucocorticoids, yet patients often have normal cortisol levels despite inflammation.
Purpose of the Study:
- To investigate the relationship between CBG cleavage and RA disease activity.
- To test the hypothesis that impaired CBG cleavage limits free cortisol delivery to RA-affected joints.
Main Methods:
- A prospective, cross-sectional observational study involving 53 RA patients and 73 healthy controls.
- Measurements included total CBG, high-affinity (haCBG) and low-affinity (laCBG) CBG, total and free cortisol, inflammatory markers (IL-6sR), and disease activity scores (DAS28).
Main Results:
- RA patients had significantly lower laCBG levels compared to healthy controls (153 vs. 191 nmol/l).
- Higher RA disease activity correlated with increased total and haCBG, and decreased free cortisol.
- CBG cleavage was reduced in RA patients and further diminished with increased disease severity.
Conclusions:
- Patients with RA exhibit reduced CBG cleavage compared to healthy individuals.
- Impaired CBG cleavage and subsequent reduced cortisol delivery may perpetuate chronic inflammation in RA.
- CBG cleavage status is a potential biomarker for RA disease activity and inflammation.
More Related Videos
Related Concept Videos
01:24Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
725
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
725
01:21Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
613
Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
613
01:29Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
657
Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
657
01:20The JAK-STAT Signaling Pathway
13.8K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
13.8K
01:24T Cell Types and Functions
3.2K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.2K
01:23Rheumatic Heart Disease I: Introduction
821
Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
821