A specific antigen‐antibody interaction triggers the cellular pathophysiology of bullous pemphigoid
A specific antigen‐antibody interaction triggers the cellular pathophysiology of bullous pemphigoid
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特异性抗原抗体相互作用触发大疱性类天疱疮的细胞病理生理学
DOI：
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发表时间：
1985
影响因子：
10.3
通讯作者：
J. Stanley
中科院分区：
文献类型：
--
作者：
J. Stanley
在大疱性类天疱疮（BP）患者的皮肤和血清中发现的自身抗体能够启动这种疾病中发生的水疱形成的病理生理学。目前的BP病理生理学概念表明，抗体本身不能引起水疱形成，但抗体通过补体固定、肥大细胞脱颗粒和随后的白细胞募集到表皮基底膜起作用。这些白细胞随后释放蛋白水解酶，导致真皮-表皮分离。本文探讨了基底膜区是否有特定分子参与了触发BP细胞病理生理的抗原-抗体反应。用[35S]蛋氨酸或14C标记的氨基酸放射标记培养的人或小鼠表皮细胞提取物的免疫沉淀物表明，26名BP患者中有25名患者的血清沉淀了相同的分子，这是通过十二烷基硫酸钠（SDS）聚丙烯酰胺凝胶电泳（PAGE）的共迁移来确定的。该分子是一种分子量约为230kd的蛋白质。通过免疫过氧化物酶对SDS - PAGE分离的蛋白进行染色，然后电泳转移到硝化纤维素片上，在正常人表皮的SDS提取物中发现了类似的蛋白。因此，在几乎所有的BP病例中，表皮基底膜的一个特定分子参与抗原-抗体相互作用，触发水疱形成的细胞病理生理。
Autoantibodies found in both the skin and sera of patients with bullous pemphigoid (BP) are capable of initiating the pathophysiology of blister formation that occurs in this disease. Current concepts of the pathophysiology of BP suggest that antibody alone cannot cause blister formation, but that antibody acts through complement‐fixation, degranulation of mast cells and subsequent recruitment of leukocytes to the epidermal basement membrane. These leukocytes then release proteolytic enzymes which result in dermal‐epidermal separation. This paper addresses the question of whether a specific molecule in the basement membrane zone is involved in the antigen‐antibody reaction which triggers the cellular pathophysiology of BP. Immunoprecipitates of extracts of cultured human or mouse epidermal cells, radiolabelled with either [35S] methionine or 14C‐labelled amino acids, indicated that sera from 25 of 26 BP patients precipitated the same molecule, as determined by co‐migration on sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis (PAGE). This molecule is a protein with a mol. wt. of approximately 230 kd. A similar protein was identified in SDS extracts of normal human epidermis, as determined by immunoperoxidase staining of proteins separated by SDS‐PAGE, then electrophoretically transferred to nitrocellulose sheets. Thus, in almost all cases of BP, one specific molecule of the epidermal basement membrane is involved in the antigen‐antibody interaction that triggers the cellular pathophysiology of blister formation.
影响因子：
6.5
作者：
GAMMON, WR;MERRITT, CC;WHEELER, CE
通讯作者：
WHEELER, CE