Advances in pemphigus research, signaling, and acantholysis

被引:0
|
作者
Bektas, M. [1 ]
Runager, K. [1 ]
Petersen, J. S. [1 ,4 ]
Rubenstein, D. S. [1 ,2 ,3 ]
机构
[1] Univ N Carolina, Sch Med, Dept Dermatol, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA
[3] Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
[4] Aarhus Univ, Dept Mol Biol, Ctr Insoluble Prot Struct inSPIN, DK-8000 Aarhus, Denmark
来源
基金
美国国家卫生研究院;
关键词
Pemphigus; Blister; Skin diseases; HEAT-SHOCK-PROTEIN; P38 MAP KINASE; LINKED IMMUNOSORBENT ASSAYS; VULGARIS-IGG; DESMOGLEIN; INOSITOL 1,4,5-TRISPHOSPHATE; ANTI-DSG1; AUTOANTIBODIES; MEDIATED PHOSPHORYLATION; INTRACELLULAR CALCIUM; KERATINOCYTE ADHESION;
D O I
暂无
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Pemphigus is a family of human autoimmune blistering diseases in which pathogenic autoantibodies induce blistering in skin and mucosa. The mechanisms by which pemphigus autoantibodies induce disease in the skin is under active investigation. A large number of cellular events induced in the target keratinocytes by pemphigus IgG have been described and suggest that pemphigus IgG binding to desmogleins trigger a complicated cascade of intracellular signaling and regulatory events. Targeting these intracellular events may prove useful therapeutically.
引用
收藏
页码:675 / 687
页数:13
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