相关实验视频
Updated: Jul 7, 2025

12:59
Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
34.5K
在牛皮中IL17和IL23抑制剂之间的类间切换:现实生活,长期,单中心体验
Silvia Giordano1, Paolo Dapavo1, Michela Ortoncelli1
1Dermatology Clinic, Medical Sciences Department, University of Turin, 10121 Torino, Italy.
Journal of clinical medicine
|December 23, 2023
概括
在IL-17治疗后切换到Interleukin-23 (IL-23) 抑制剂对于牛皮是有效的. 这项研究显示了显著的PASI得分降低和持续的结果,IL-23抑制剂为中度至重症牛皮患者提供了安全的替代方案.
科学领域:
- 皮肤病学 皮肤病学
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 干白素-23 (IL-23) 抑制剂对牛皮有效.
- 患有牛皮的患者可能会经历IL-17抑制剂治疗失败.
- 在IL-17治疗后对IL-23抑制剂的疗效存在有限的数据.
研究的目的:
- 为了评估IL-23抑制剂在中度至重度牛皮症患者的有效性,这些患者从IL-17抑制剂转换.
- 评估这种治疗开关的安全性和长期结果.
主要方法:
- 一项涉及48名中度至重度牛皮病患者的研究.
- 患者从IL-17抑制剂转换为IL-23抑制剂.
- 该试验被注册为SS_DERMO_20.
主要成果:
- 平均PASI分数在第16周从11.6下降到3.3,持续到第52周.
- 超过24%的人在16周达到PASI100,在48周达到61.9%.
- 没有报告严重的不良事件,尽管16%的患者因不有效而停止服用IL-23抑制剂.
结论:
- 在IL-17和IL-23抑制剂之间切换是一种安全有效的牛皮管理策略.
- IL-23抑制剂对于那些对IL-17药物无反应的患者来说是一个可行的替代品.
- 持续的疗效和安全性档案支持这种类间切换在牛皮治疗中.
相关概念视频
T Cell Types and Functions
1.0K
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...
1.0K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
141
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...
141
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
121
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...
121
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
168
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...
168
Inflammatory Bowel Disease IV: Pharmacological Management
128
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...
128
The JAK-STAT Signaling Pathway
8.9K
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...
8.9K

