Altered leukocyte protein kinase activity in atopic dermatitis.
Altered leukocyte protein kinase activity in atopic dermatitis.
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特应性皮炎中白细胞蛋白激酶活性的改变。
DOI：
10.1111/1523-1747.ep12461047
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Hanifin,JM
中科院分区：
文献类型：
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作者：
Trask,DM;Chan,SC;Sherman,SE;Hanifin,JM
先前的研究表明，特应性皮炎(AD)患者的单核白细胞(MNL)中环-AMP特异性磷酸二酯酶(PDE)活性升高。我们质疑增加的激酶活性是否可以解释这一观察结果。在这些研究中，我们测量了AD患者MNL中基础钙/磷脂依赖性蛋白激酶(PK-C)异常低的磷酸化水平。AD患者MNL中基础cAMP依赖的蛋白激酶(PK-A)磷酸化水平明显升高。这些结果与早期的报道一致，即PR-A活性可能对某些细胞系统中的PK-C活性有负面影响。用H1-组胺激动剂噻唑乙胺(TEA)刺激正常供者的MNL，而不是AD患者的MNL，导致PK-C磷酸化显著增加。这意味着AD细胞中的受体下调或功能脱敏。基础蛋白激酶磷酸化改变和对选择性组胺激动剂的异常反应可以解释AD患者MNL中PDE活性升高的原因。
Previous studies have demonstrated elevated cyclic-AMP- specific phosphodiesterase (PDE) activity in mononuclear leukocytes (MNL) from patients with atopic dermatitis (AD). We questioned whether increased kinase activation could account for this observation. In these studies, we measured abnormally lower basal calcium/phospholipid-dependent protein kinase (PK-C) phosphorylation in MNL from patients with AD. Basal cAMP-dependent protein kinase (PK-A) phosphorylation was concomitantly higher in MNL from patients with AD. These results are in agreement with earlier reports that PR-A activity may have a negative influence on PK-C activity in certain cell systems. Stimulation with the H1-histamine agonist, thiazolylethylamine (TEA), of MNL from normal donors but not patients with AD, resulted in statistically significant increases in PK-C phosphorylation. This implies receptor down regulation or functional desensitization in AD cells. Altered basal protein kinase phosphorylation and abnormal response to selective histamine agonists seen in MNL from patients with AD could explain elevated PDE activity.