甲托雷克萨特用于耐火性成人亚托皮性皮肤炎导致皮肤IL-31和IL-31RA表达的改变
Luciana Paula Samorano1, Kelly Cristina Gomes Manfrere2, Naiura Vieira Pereira2
1Department of Dermatology, Faculty of Medicine, Universidade de São Paulo, São Paulo, SP, Brazil.
Anais brasileiros de dermatologia
|September 20, 2023
概括
甲托雷克萨特 (MTX) 治疗减少了皮肤厚度,改变了炎症标志物,特别是IL-31和IL-31RA,在患有中度/重度亚托皮炎 (AD) 的成年人中. 这项研究提供了对MTX的见解.
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:
- 亚托皮炎 (AD) 是一种慢性炎症性皮肤疾病.
- 甲托雷克萨特 (MTX) 作为适度/严重AD的替代治疗.
- 了解MTX对AD皮肤的分子作用对于优化治疗至关重要.
研究的目的:
- 评估甲状腺素对成年AD患者中细胞因子和化学因子的表达的影响.
- 在MTX治疗24周后,评估炎症标志物的变化.
- 调查MTX对表皮厚度和与炎症和有关的特定基因/蛋白质表达的影响.
主要方法:
- 一项前性队列研究,涉及12名患有中度/重度AD的成年人,接受口服MTX (15毫克/周24周) 治疗.
- 与10个非atopic匹配的对照进行了比较.
- 对治疗前和后的皮肤活检 (损伤和非损伤) 的分析,检查表皮厚度和IL-31,IL-31RA,OSMR,TSLP,Ki67,IL-4,IL-6,IL-10,TNF-α,IFN-γ,TARC和CCL-22的表达.
主要成果:
- 在MTX治疗后的病变性AD皮肤中,平均表皮厚度显著减少 (p=0.021).
- 在表皮中增加IL-31RA表达 (免疫组织化学) (p=0.016).
- 在MTX治疗后的病变性AD皮肤中减少IL-31基因表达 (p=0.019). 对于其他标记物,没有观察到显著变化.
结论:
- 在中度/重度AD的成年人中,甲托雷克萨治疗有效地减少了表皮性增生症.
- MTX改变了炎症性细胞因子和受体的皮肤表达,特别是与有关的细胞因子,如IL-31和IL-31RA.
- 研究的局限性包括样本规模小,随访时间短.
相关概念视频
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
190
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...
190
T Cell Types and Functions
1.1K
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...
1.1K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
168
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...
168
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
144
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...
144
Inflammatory Bowel Disease IV: Pharmacological Management
152
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...
152
Antiasthma Drugs: Leukotriene Modifiers
343
Leukotriene modifiers, or cysteinyl leukotriene receptor antagonists, are medications used to manage chronic asthma. These agents target specific inflammatory mediators produced during arachidonic acid metabolism, an essential process in generating inflammation in the body.
Leukotriene modifiers work through two distinct mechanisms:
Leukotriene modifiers work through two distinct mechanisms:
343


