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白细胞的酸化p38 MAP激酶表达在过敏的人群中增加,并与IgE反应相关
Jonathan I Silverberg1, Tamar A Smith-Norowitz2, Stephan Kohlhoff2
1Department of Dermatology, George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.
Scandinavian journal of immunology
|March 5, 2024
概括
酸化p38基因激活蛋白激酶 (MAPK) 与过敏个体的免疫球蛋白E (IgE) 水平较高有关. 抑制这种途径显著降低了IgE的产生,这表明p38 MAPK是潜在的抗过敏药物标.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞信号传递 细胞信号传递
- 分子生物学分子生物学
背景情况:
- 线素激活蛋白激酶 (MAPK) 调节重要的细胞过程,如增殖,分化和亡.
- 酸化的p38 MAPK (phos-p38 MAPK) 参与Th2细胞因子反应和免疫球蛋白E (IgE) 的产生.
- 在IgE生产中MAPK通路的确切作用尚未完全阐明.
研究的目的:
- 研究MAPK通路 (p38,ERK,JNK) 与过敏个体的IgE产生之间的关联.
- 为了确定phos-p38 MAPK是否是一种潜在的过敏治疗点.
主要方法:
- 流细胞计和微酶免疫试验被用来测量血白细胞子集和血清Ig水平中的phos-p38,ERK和JNK MAPK表达在患有或没有喘/鼻结炎的成年人中.
- 来自过敏患者的外周血液单核细胞 (PBMC) 用抗CD40/复合IL-4进行培养,有或没有-p38MAPK抑制剂 (SB202190).
- 用ELISA量化了培养超水体中的IgE水平.
主要成果:
- 白细胞中的-p38 MAPK表达与过敏患者的血清IgE水平显著相关 (p ≤0.01),独立于混因素.
- 白细胞表达的phos-ERK和JNK与IgE没有相关性,但phos-ERK与血清IgG相关.
- 在体外,-p38 MAPK 抑制剂 SB202190 以剂量依赖的方式 (高达 82.1% 的抑制) 以最小的细胞毒性抑制了 PBMC 的 IgE 生产.
结论:
- 不同的MAPK通路与IgE (p38) 和IgG (ERK) 反应有不同的关联.
- -p38 MAPK在调节IgE产生方面发挥着重要作用.
- -p38 MAPK代表了抗过敏药物开发的有希望的治疗标.
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