Characterization of cAMP‐phosphodiesterase as a possible laboratory marker of atopic dermatitis

Characterization of cAMP‐phosphodiesterase as a possible laboratory marker of atopic dermatitis
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cAMP-磷酸二酯酶作为特应性皮炎可能实验室标志物的表征

DOI:
10.1002/ddr.430130205
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发表时间:
1988
影响因子:
3.8
通讯作者:
S. Chan
S. Chan
中科院分区:
医学3区
文献类型:
--
作者:
J. Hanifin;S. Chan

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特应性皮炎(AD)是一种慢性复发性皮肤炎性疾病,可影响高达10%的人口。这种情况是特应性三联征的一部分,其中还包括哮喘和过敏性鼻炎。这些疾病有很强的遗传模式,但遗传学尚不清楚。AD的特征在于多种免疫学和药理学异常,并且来自移植研究的证据表明基本异常在骨髓细胞中表达。缺陷如嗜碱性粒细胞组胺释放增加和B淋巴细胞自发性IgE产生高意味着细胞调节缺陷。已证实AD患者环核苷酸代谢异常,cAMP-磷酸二酯酶(PDE)升高导致细胞内cAMP水平降低,可能对免疫和炎症反应产生净容许效应。AD患者单核白细胞中异常PDE的生化表征研究表明,PDE活性的两个明显异常的胞浆组分。这些可能代表了单核细胞和淋巴细胞中不同的酶形式;这些免疫重要细胞的调节异常可能解释了许多与AD相关的免疫异常,并可能为流行病学,遗传学和临床研究提供急需的生化标志物。
Atopic dermatitis (AD) is a chronically recurrent cutaneous inflammatory disease which may affect up to 10% of the population. The condition is part of the atopic triad which also includes asthma and allergic rhinitis. These diseases have strong hereditary patterns but the genetics is unclear. AD is characterized by a variety of immunologic and pharmacologic abnormalities, and evidence from transplant studies indicates that the basic abnormality is expressed in bone marrow cells. Defects such as increased basophil histamine release and high spontaneous IgE production by B lymphocytes imply defective cellular regulation. Abnormalities of cyclic nucleotide metabolism have been demonstrated in AD, and elevated cAMP‐phosphodiesterase (PDE) with resultant low intracellular cAMP levels may have a net permissive effect on immune and inflammatory responses. Biochemical characterization studies of abnormal PDE in mononuclear leukocytes from patients with AD have demonstrated two distinctly abnormal cytosolic fractions of PDE activity. These probably represent different enzyme forms in monocytes and lymphocytes; the consequent dysregulation of these immunologically important cells may explain many of the immune abnormalities associated with AD, and may provide a much needed biochemical marker for epidemiologic, genetic and clinical studies.
白细胞的异源脱敏:特应性皮炎中β肾上腺素能阻断的可能机制。
DOI: 10.1016/0091-6749(81)90187-1
发表时间: 1981
期刊: The Journal of allergy and clinical immunology
影响因子: --
作者:
Safko,MJ;Chan,SC;Cooper,KD;Hanifin,JM
通讯作者: Hanifin,JM
Ro 20-1724 抑制磷酸二酯酶可减少体外特应性皮炎细胞的高 IgE 合成。
DOI: 10.1111/1523-1747.ep12272486
发表时间: 1985
期刊: The Journal of investigative dermatology
影响因子: --
作者:
Cooper,KD;Kang,K;Chan,SC;Hanifin,JM
通讯作者: Hanifin,JM
特应性皮炎中白细胞对磷酸二酯酶抑制剂的敏感性增加:茶碱治疗后快速耐受。
DOI: 10.1016/0091-6749(84)90254-9
发表时间: 1984
期刊: The Journal of allergy and clinical immunology
影响因子: --
作者:
Giustina,TA;Chan,SC;Thiel,ML;Baker,JW;Hanifin,JM
通讯作者: Hanifin,JM
患有特应性皮炎的儿童在食物挑战后血浆组胺浓度升高。
DOI: 10.1056/nejm198408093110605
发表时间: 1984
期刊: The New England journal of medicine
影响因子: --
作者:
Sampson,HA;Jolie,PL
通讯作者: Jolie,PL
由于刺激人单核白细胞中的环 AMP-磷酸二酯酶而导致功能脱敏。
DOI: --
发表时间: 1982
期刊: Journal of cyclic nucleotide research
影响因子: --
作者:
Chan,SC;Grewe,SR;Stevens,SR;Hanifin,JM
通讯作者: Hanifin,JM