Related Experiment Video
Updated: Aug 12, 2026
08:43
Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice
Published on: January 31, 2020
Anti-interleukin-1 therapy in rheumatic diseases
J M Dayer1, U Feige, C K Edwards
1Division of Immunology and Allergy, University Hospital, Geneva, Switzerland. Jean-Michel.Dayer@hcuge.ch
Current Opinion in Rheumatology
|May 3, 2001
Summary
Interleukin-1 receptor antagonist (IL-1Ra) effectively treats rheumatoid arthritis (RA) by blocking interleukin-1 (IL-1). Clinical studies show IL-1Ra reduces RA symptoms, slows bone damage, and is safe for patients.
Area of Science:
- Immunology
- Rheumatology
- Pharmacology
Background:
- Interleukin-1 (IL-1) is a key cytokine in initiating rheumatoid arthritis (RA) pathogenesis.
- The body's natural defense, IL-1 receptor antagonist (IL-1Ra), effectively neutralizes IL-1 activity.
- Preclinical studies demonstrated that IL-1 inhibition benefits RA outcomes.
Purpose of the Study:
- To evaluate the clinical efficacy and safety of IL-1Ra in treating rheumatoid arthritis.
- To determine if IL-1Ra can slow the radiographic progression of joint damage in RA patients.
Main Methods:
- Two large, well-controlled clinical studies were conducted in patients with rheumatoid arthritis.
- The studies assessed the clinical effectiveness of IL-1Ra.
- Radiographic measurements were used to evaluate the progression of bone damage.
Main Results:
- IL-1Ra was found to be clinically effective in treating rheumatoid arthritis.
- IL-1Ra significantly reduced the signs and symptoms of RA.
- Radiographic analysis indicated that IL-1Ra slows the progression of bone damage.
Conclusions:
- IL-1Ra is a clinically effective treatment for rheumatoid arthritis.
- IL-1Ra offers a specific and selective approach to inhibiting the IL-1 pathway in RA.
- IL-1Ra demonstrates a favorable safety and tolerability profile, making it a promising therapeutic option for RA.
Related Concept Videos
01:20The JAK-STAT Signaling Pathway
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...
01:24T Cell Types and Functions
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...
01:29Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
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 Disease...
01:24Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
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 (Humira),...
01:21Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
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 (COX-2),...
01:29Inflammatory Bowel Disease IV: Pharmacological Management
Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Pharmacologic...