ライフサイエンスコーパス: acantholysis

1 haracterized by detachment of keratinocytes (acantholysis).

2 g3), causing epidermal cell-cell detachment (acantholysis).

3 mportant component of pemphigus IgG-mediated acantholysis.

4 8MAPK and apoptosis may not be essential for acantholysis.

5 leased Src activity in intact KCs and caused acantholysis.

6 signaling and that this process may lead to acantholysis.

7 anistic role for signaling in PV IgG-induced acantholysis.

8 ized skin also had crusting and suprabasilar acantholysis.

9 ay by which pemphigus autoantibodies lead to acantholysis.

10 mosomal cadherin, DSG3 (desmoglein-3), cause acantholysis.

11 sequence of, p38MAPK activation in pemphigus acantholysis.

12 tology typical of PV, including suprabasilar acantholysis and "tombstoning" of basal cells.

13 IVIg reduced PV IgG-mediated acantholysis and cell death and up-regulated the caspase

14 olinergic agonists to inhibit PV IgG-induced acantholysis and phosphorylation of KC adhesion molecule

15 gross skin blisters with PV-like suprabasal acantholysis and stained perilesional epidermis in a fis

16 To further understand acantholysis and the efficacy of IVIg, we measured effec

17 by loss of adhesion between epidermal cells (acantholysis) and abnormal keratinization.

18 by loss of adhesion between epidermal cells (acantholysis) and abnormal keratinization.

19 smoglein-1 induce epidermal cell detachment (acantholysis) and blistering.

20 al loss of adhesion between epidermal cells (acantholysis) and by abnormal keratinization.

21 vulgaris patients leads to skin blistering (acantholysis) and oral mucosa lesions.

22 zed by subcorneal epidermal cell detachment (acantholysis) and pathogenic autoantibodies against desm

23 skin and oral mucosa), histology (epidermal acantholysis), and immunological abnormalities (circulat

24 ules clinically and lower epidermal blister, acantholysis, and neutrophilic infiltration pathological

25 acterized by blister at the lower epidermis, acantholysis, and neutrophilic infiltration.

26 detachment within the stratified epithelium (acantholysis) caused by IgG autoantibodies.

27 ylprednisolone (MP) can block PV IgG-induced acantholysis, decreasing the extent of keratinocyte deta

28 The extent of acantholysis in KC monolayers correlated closely with th

29 rmis in a pemphigus-like pattern and induced acantholysis in keratinocyte monolayers.

30 lity of the same drug combination to abolish acantholysis in mouse skin.

31 mice, but not WT mice, induces suprabasilar acantholysis in mucosal tissues, thus confirming the pat

32 tored acantholytic activity, indicating that acantholysis in PV results from synergistic action of an

33 We speculate that ulceration occurs after acantholysis in the fragile epidermis because environmen

34 The epidermis is fragile, and acantholysis in the granular layer generates localized l

35 The skin showed hyperplasia and acantholysis in the mid- and lower epidermal layers, whe

36 ary for pemphigus immunoglobulin G to induce acantholysis in the neonatal mouse model of pemphigus.

37 s immunoglobulin G caused gross blisters and acantholysis in the superficial and suprabasal epidermis

38 omes due to steric hindrance, thus rendering acantholysis irreversible.

39 ratinization (epidermal differentiation) and acantholysis (loss of cohesion) of keratinocytes.

40 ition to the dramatic skin and mucocutaneous acantholysis observed in pemphigus patients.

41 an produce pathogenic Abs capable of causing acantholysis of human foreskin in culture and blistering

42 characterized by suprabasal cell separation (acantholysis) of the epidermis.

43 e that in different PV patients, IgG-induced acantholysis proceeds predominantly via distinct, yet co

44 y and trafficking and pemphigus IgG-mediated acantholysis, providing further insights into the comple

45 inhibitors demonstrated that PV IgGs induced acantholysis through both pathways.

46 n addition, electron microscopy demonstrated acantholysis throughout all layers of the skin, focal de

47 (PV) can induce keratinocyte (KC) dyshesion (acantholysis) via mechanisms that involve signaling kina

48 To determine whether acantholysis was related to a defect in the number or as

49 reversible, leading to epidermal blistering (acantholysis), when AMA synergize with anti-Dsg antibodi

50 tivation is part of the mechanism leading to acantholysis, whereas the later peak of p38MAPK and apop

51 anti-alpha9 antibody induced pemphigus-like acantholysis, which could be reversed either spontaneous