用特拉洛基努马布向IL-13将在早期和2年后的阿托皮性皮炎中使2型炎症正常化
Emma Guttman-Yassky1, Kenji Kabashima2, Delphine Staumont-Salle3
1Department of Dermatology and the Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Allergy
|April 2, 2024
概括
特拉洛金马布有效中和介素-13,改善皮肤生物标志物和表皮病理在成年人与阿托皮性皮炎 (AD). 长期治疗将关键基因表达转向非损伤水平,证实IL-13的存在.
科学领域:
- 免疫皮肤学 免疫皮肤学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 亚托匹性皮肤炎 (AD) 是由皮肤炎症和屏障功能障碍驱动的,受到中白素-13 (IL-13) 的显著影响.
- 一种单克隆抗体的特拉洛基努马布 (tralokinumab) 特别准和中和IL-13.
研究的目的:
- 评估通过特拉洛基努马布对皮肤和血清生物标志物的IL-13中和的早期和长期 (2年) 影响,在中度至重度AD的成年人中.
- 评估特拉洛金马布对损伤性皮肤和全身炎症标志物中的基因和蛋白质表达的影响.
主要方法:
- 分析ECZTRA 1和ECZTEND试验中患者的皮肤活检和血液样本.
- 使用RNA测序和蛋白质分析通过免疫组织化学和免疫测试进行基因表达概况.
主要成果:
- 特拉洛基努马布迅速改善了皮肤转录组形状,并在16周后减少了39%的失调基因表达,并在2年后减少了85%.
- 在16周观察到2型血清生物标志物 (CCL17/TARC,皮质素,IgE) 和表皮厚度显著降低.
- 两年的治疗使关键Th2,Th1和Th17/Th22通路基因的表达正常化,并增加了表皮分化标志物.
结论:
- 特拉洛金马布治疗有效地改善表皮病理,并减少AD的系统性2型炎症标志物.
- 该药物将皮肤中的AD生物标志物转移到非损伤水平,强调IL-13在AD病变发生过程中的中心作用.
更多相关视频
03:40Acupoint Catgut Embedding Therapy in Traditional Chinese Medicine for Managing Allergic Rhinitis
Published on: December 20, 2024
461
06:15Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay
Published on: September 7, 2018
9.4K
相关概念视频
01:24T 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
01:24Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
137
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...
137