ライフサイエンスコーパス: blistering

1 adjunctive therapy for control of pemphigus blistering.

2 expression, and GM-CSF blockade reduced skin blistering.

3 educed fibulin-2 and did not appear to cause blistering.

4 dermis of wounds, characterized by extensive blistering.

5 -mediated inhibition of DSG3 binding to skin blistering.

6 bsequent MC degranulation, and ultimately BP blistering.

7 r/Thr), also bound Dsg1 and blocked the skin blistering.

8 Ab could prevent keratinocyte detachment and blistering.

9 lustrated in a patient with mucosal-dominant blistering.

10 nocyte layer), leading to cell fragility and blistering.

11 epidermal cell detachment (acantholysis) and blistering.

12 ak of p38MAPK activation but failed to block blistering.

13 desmoglein-1-specific autoantibodies induce blistering.

14 rized by oral mucosal erosions and epidermal blistering.

15 immune disease characterized by subepidermal blistering.

16 tinocytes leading to epidermal cytolysis and blistering.

17 ing in severe mucosal erosions and epidermal blistering.

18 culating pathogenic IgG levels and prevented blistering.

19 hil infiltration and subsequent subepidermal blistering.

20 rmolysis bullosa simplex with intraepidermal blistering.

21 to induce painful cutaneous inflammation and blistering.

22 late onset of mild skin fragility and acral blistering.

23 underlying pathophysiology of inherited skin blistering.

24 icantly reduced PAO-induced inflammation and blistering.

25 rsenicals-induced cutaneous inflammation and blistering.

26 3) IgG autoantibodies cause life-threatening blistering.

27 prophylactic IL-1ra administration prevented blistering.

28 We used skin suction blistering, a painless and nonscarring procedure that ca

29 in pemphigus vulgaris patients leads to skin blistering (acantholysis) and oral mucosa lesions.

30 ey become irreversible, leading to epidermal blistering (acantholysis), when AMA synergize with anti-

31 Finally, we also demonstrate that the blistering activity associated with pederin and other me

32 mide, psymberin does not display irritant or blistering activity.

33 rfare agents (organophosphorus nerve agents, blistering agents, and their simulants) and toxic indust

34 mpaired intercellular adhesion and epidermal blistering also occur in individuals with pemphigus (whi

35 In addition to blistering and a severe disorder of cornification, patie

36 DEB disease features, including subepidermal blistering and anchoring fibril defects.

37 rast, other instabilities of sheets, such as blistering and cracking, break the homogeneity of shape

38 (EB) are characterized by chronic, lifelong blistering and erosions due to mutations in 10 distinct

39 osa is a family of diseases characterized by blistering and fragility of the skin in response to mech

40 c atresia (EB-PA), manifesting with neonatal blistering and gastric anomalies, is known to be caused

41 mice, beta1 mutant mice exhibit severe skin blistering and hair defects, accompanied by massive fail

42 e within 10 days after birth, accompanied by blistering and hyperproliferation in the epithelia, simi

43 ries, V-series, and "new" nerve agents), and blistering and incapacitating warfare agents.

44 hanism underlying lewisite-induced cutaneous blistering and inflammation and describe its novel antid

45 e not usually associated with prominent skin blistering and keratin filament clumping.

46 this disease is characterized by severe skin blistering and pathogenic anti-desmoglein-1 (Dsg1) autoa

47 hyria and (2) cutaneous porphyrias with skin blistering and photosensitivity: porphyria cutanea tarda

48 l substrate and a protective oxide can cause blistering and spallation of the scale.

49 ility of pathogenic pemphigus IgGs to induce blistering and that both p38 mitogen-activated protein k

50 molysis bullosa (EB) is associated with skin blistering and the development of chronic nonhealing wou

51 Integrin loss in vertebrate skin leads to blistering and wound healing defects.

52 kin barrier defect with epidermal abrasions, blistering, and early postnatal lethality, due to a thin

53 hen homozygous exhibits oral leukoplakia and blistering, and growth retardation.

54 onal blebbing but not late apoptotic events, blistering, and lysis.

55 ed disorder characterized by skin fragility, blistering, and multiple skin wounds with no currently a

56 ntation, pliability, raised scar, epithelial blistering, and surface texture.

57 cture of tungsten, leading to bubble growth, blistering, and/or to the formation of fuzz.

58 attractive option for the prevention of skin blistering associated with K14 mutations in EBS.

59 erized by generalized erythema and cutaneous blistering at birth followed by hyperkeratosis and less

60 yperactivated mutant alphaPS2 proteins cause blistering at expression levels well below those require

61 oimmune disease with severe and chronic skin blistering, autoantibodies are directed against type VII

62 pemphigoid (MMP) is a heterogeneous group of blistering autoimmune disorders of unknown etiology.

63 OCP is a subepithelial, blistering, autoimmune disease that mainly affects the c

64 Suction blistering captured epidermal and most immune cells equa

65 nct transcriptional programs, alleviates the blistering caused by a K14 deficiency in an EBS mouse mo

66 s a disorder of incurable skin fragility and blistering caused by mutations in the type VII collagen

67 Transient embryonic epidermal blistering causes the characteristic defects of the diso

68 Arsenicals are painful, inflammatory and blistering causing agents developed as chemical weapons

69 he inability of K16 to fully rescue the skin blistering characteristic of K14 null mice.

70 rmatitis herpetiformis (DH) is an autoimmune blistering condition seen in the context of celiac disea

71 on, with different phenotypes, including the blistering conditions Stevens-Johnson syndrome (SJS) and

72 FINDINGS: MMP is an uncommon, subepithelial blistering conjunctivitis that is commonly associated wi

73 isorder characterized by embryonic epidermal blistering, cryptophthalmos, syndactyly, renal defects a

74 246D and D392N) responsible for a C. elegans blistering cuticle phenotype was also investigated.

75 Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody

76 nce of gastro-oesophageal reflux disease and blistering/desquamating skin disorder respectively in fe

77 ternative pathway in an autoantibody-induced blistering disease and should facilitate the development

78 Using an IgA-dependent skin-blistering disease as a model system, we demonstrated co

79 phigoid (BP) is an inflammatory subepidermal blistering disease associated with an IgG autoimmune res

80 Bullous pemphigoid (BP) is a subepidermal blistering disease associated with autoantibodies agains

81 emphigoid (BP) is an autoimmune subepidermal blistering disease associated with autoantibodies direct

82 Pemphigus vulgaris is a blistering disease associated with autoantibodies to the

83 rmolysis bullosa acquisita is a subepidermal blistering disease associated with tissue-bound and circ

84 the major autoantigen of the autoimmune skin blistering disease bullous pemphigoid.

85 mphigus vulgaris (PV) is a potentially fatal blistering disease caused by autoantibodies (autoAbs) ag

86 Pemphigus foliaceus (PF) is a blistering disease caused by autoantibodies to desmoglei

87 a is an incurable, often fatal mucocutaneous blistering disease caused by mutations in COL7A1, the ge

88 ophic epidermolysis bullosa is a devastating blistering disease caused by mutations in the COL7A1 gen

89 mphigus vulgaris (PV) is a potentially fatal blistering disease characterized by autoantibodies again

90 garis (PV) is a potentially fatal autoimmune blistering disease characterized by autoantibodies again

91 mphigus vulgaris (PV) is a potentially fatal blistering disease characterized by autoantibodies again

92 f pemphigus foliaceus (PF), is an autoimmune blistering disease characterized by autoantibodies again

93 Bullous pemphigoid (BP) is a subepidermal blistering disease characterized by autoantibodies again

94 pemphigoid is a rare subepidermal autoimmune blistering disease characterized by autoantibodies again

95 s pemphigoid (BP), a subepidermal autoimmune blistering disease characterized by autoantibodies direc

96 or cicatricial pemphigoid is a mucocutaneous blistering disease characterized by autoantibodies to di

97 Pemphigus vulgaris (PV) is an autoimmune blistering disease characterized by autoantibodies to th

98 quisita (EBA) is an autoimmune sub-epidermal blistering disease characterized by autoantibodies to ty

99 sis bullosa acquisita (EBA) is an autoimmune blistering disease characterized by autoantibodies to ty

100 s (PV) is a potentially lethal mucocutaneous blistering disease characterized by cell-cell detachment

101 Bullous pemphigoid (BP) is a subepidermal blistering disease characterized by IgE and IgG class au

102 s (PV) is a potentially lethal mucocutaneous blistering disease characterized by IgG autoantibodies (

103 ullous pemphigoid (BP) is an autoimmune skin-blistering disease characterized by the presence of auto

104 oped a delayed and significantly less severe blistering disease compared with factor B-sufficient mic

105 II collagen into mice induces a subepidermal blistering disease dependent upon activation of terminal

106 ysis bullosa acquisita is an autoimmune skin-blistering disease driven by autoantibodies to type VII

107 e dystrophic epidermolysis bullosa (RDEB), a blistering disease due to defective extracellular type V

108 ead to the severe recessive form of the skin blistering disease dystrophic epidermolysis bullosa (RDE

109 ngs from 51 patients with the inherited skin-blistering disease epidermolysis bullosa (EB), we show t

110 A characteristic feature of the skin blistering disease epidermolysis bullosa simplex is kera

111 econstitution with granulocytes restored the blistering disease in factor B-deficient mice.

112 at provide care for patients with autoimmune blistering disease in Germany, Italy, Singapore, Israel,

113 report that p38MAPK inhibitors prevented PV blistering disease in vivo.

114 mphigus foliaceus (PF) is a human autoimmune blistering disease in which a humoral immune response ta

115 Pemphigus vulgaris (PV) is an autoimmune blistering disease in which antibodies against the desmo

116 gus vulgaris (PV) is an autoimmune epidermal blistering disease in which autoantibodies (IgG) are dir

117 molysis bullosa simplex (EBS-DM) is a severe blistering disease inherited in an autosomal-dominant fa

118 mphigus foliaceus (PF) is an autoimmune skin blistering disease mediated by pathogenic autoantibodies

119 Hailey-Hailey disease is a severe genetic blistering disease of intertriginous skin locations that

120 Pemphigus vulgaris (PV) is an autoimmune blistering disease of skin and mucous membranes caused b

121 sis bullosa acquisita (EBA) is an autoimmune blistering disease of the skin and mucous membranes, cha

122 ermolysis bullosa acquisita is an autoimmune blistering disease of the skin characterized by IgG auto

123 In the human autoimmune blistering disease pemphigus vulgaris (PV) pathogenic an

124 In the autoimmune skin-blistering disease pemphigus vulgaris (PV), autoantibodi

125 otal factor for initiation of the autoimmune blistering disease pemphigus.

126 Patients with the genetic skin blistering disease recessive dystrophic epidermolysis bu

127 encoding collagen VII cause the devastating blistering disease recessive dystrophic epidermolysis bu

128 Patients with autoimmune blistering disease seem to have a lower risk of PCP than

129 potentially fatal IgG autoantibody-mediated blistering disease targeting mucocutaneous keratinocytes

130 pemphigoid (BP) is an autoantibody-mediated blistering disease that is often associated with neurolo

131 llosa is an autosomal recessive subepidermal blistering disease typified by null mutations in COL17A1

132 These mutant mice develop a progressive blistering disease validated at the gross and microscopi

133 from autoantibody-induced arthritis and skin blistering disease, as well as from the reverse passive

134 sis bullosa acquisita (EBA) is an autoimmune blistering disease, characterized by antibodies to type

135 nce of these structures leads to the chronic blistering disease, dystrophic epidermolysis bullosa.

136 goid (BP), the most frequent autoimmune skin-blistering disease, involves matrix metalloproteinase 9

137 Bullous pemphigoid (BP), a common autoimmune blistering disease, is increasing in incidence and conve

138 ntigen in a malignancy-associated autoimmune blistering disease, paraneoplastic pemphigus.

139 ents with this potentially lethal autoimmune blistering disease.

140 ) is a chronic mucocutaneous autoimmune skin blistering disease.

141 a potentially fatal autoimmune mucocutaneous blistering disease.

142 most cases there was no family history of a blistering disease.

143 a potentially fatal autoimmune mucocutaneous blistering disease.

144 (BP) is by far the most frequent autoimmune blistering disease.

145 n desmoplakin can result in devastating skin blistering diseases and arrhythmogenic right ventricular

146 f genome editing as a therapy for congenital blistering diseases and as an antimicrobial agent, and w

147 ithelial and cardiac muscle cells cause skin-blistering diseases and cardiomyopathies.

148 antibody-induced, cell-mediated subepidermal blistering diseases and identified new therapeutic targe

149 Autoimmune blistering diseases are a heterogeneous group of about a

150 Autoimmune blistering diseases are characterized by substantial mor

151 Autoimmune blistering diseases are generally distinct entities char

152 In the blistering diseases bullous impetigo and staphylococcal

153 eing described, diagnosis of most autoimmune blistering diseases can now be achieved using standardiz

154 ) and pemphigus vulgaris (PV) are autoimmune blistering diseases characterized by autoantibodies agai

155 tis prophylaxis for patients with autoimmune blistering diseases does not seem to be warranted.

156 ry care physician to the national Center for Blistering Diseases in The Netherlands.

157 Possible resemblance of the lesions to human blistering diseases is discussed.

158 sts of a group of rare and severe autoimmune blistering diseases mediated by pathogenic autoantibodie

159 n and have implications for the treatment of blistering diseases of the skin.

160 incidence of PCP in patients with autoimmune blistering diseases receiving no routine prophylaxis.

161 during embryogenesis, and certain desmosomal blistering diseases such as pemphigus vulgaris and pemph

162 argeted by pathogenic autoantibodies in skin blistering diseases such as pemphigus.

163 A total of 801 patients with autoimmune blistering diseases were included in this study; their m

164 Pemphigus encompasses a group of autoimmune blistering diseases with circulating pathogenic autoanti

165 heir differential diagnosis of acute febrile blistering diseases, and be aware that certain patients

166 of inherited genetic diseases including skin blistering diseases, corneal opacities, and neurological

167 s bullosa (EB), a group of complex heritable blistering diseases, is the topic of triennial research

168 and its dysfunction is linked to human skin blistering diseases.

169 tments for PV and other desmosome-associated blistering diseases.

170 ntinents dedicating their work to autoimmune blistering diseases.

171 Pemphigus is an autoimmune blistering disorder associated with significant morbidit

172 Pemphigus vulgaris (PV) is an epidermal blistering disorder caused by antibodies directed agains

173 is bullosa (RDEB) is a severe inherited skin-blistering disorder caused by mutations in the COL7A1 ge

174 EB) is a devastating, often fatal, inherited blistering disorder caused by mutations in the COL7A1 ge

175 ermolysis bullosa (RDEB), a severe heritable blistering disorder caused by mutations in the type VII

176 ermolysis bullosa (RDEB) is a rare monogenic blistering disorder caused by the lack of functional typ

177 f-expression mutations cause the lethal skin blistering disorder Herlitz junctional epidermolysis bul

178 Pemphigus is a life-threatening blistering disorder of the skin and mucous membranes cau

179 implex (EBS) is an incurable, inherited skin-blistering disorder predominantly caused by dominant-neg

180 mouse model for the autosomal-dominant skin blistering disorder, epidermolytic hyperkeratosis (MIM 1

181 l epidermolysis bullosa, a lethal hereditary blistering disorder, is usually treated by palliative ca

182 The blistering disorder, lethal junctional epidermolysis bul

183 thologic diagnosis of an acquired autoimmune blistering disorder.

184 (MMP) is a heterogeneous group of autoimmune blistering disorders characterized by subepithelial sepa

185 d healthy volunteers and patients with other blistering disorders such as pemphigus vulgaris.

186 cally and genetically heterogeneous group of blistering disorders with considerable morbidity and mor

187 ullosa is a heterogeneous group of heritable blistering disorders with considerable morbidity and mor

188 rview will focus on the prototypic heritable blistering disorders, epidermolysis bullosa, and related

189 Of the genetic blistering disorders, RDEB has the highest rate of morbi

190 B among the "cell-poor" list of subepidermal blistering disorders.

191 psoriasis, allergic contact dermatitis, and blistering disorders.

192 es such as vitiligo, melanoma, psoriasis and blistering disorders.

193 effective for treating desmosome autoimmune blistering disorders.

194 in disorders characterized by intraepidermal blistering, epidermal hyperkeratosis, or abnormalities i

195 in disease manifesting with sub-lamina densa blistering, erosions, and chronic ulcers.

196 but included discomfort, cutaneous erythema, blistering, eyelash loss, and floaters; these were unifo

197 e dermo-epidermal junction lead to cycles of blistering followed by regeneration of the skin.

198 ients, and these translated into accelerated blistering following mechanically induced stress.

199 e grafts may exhibit surface instability and blistering for up to a year following grafting, and sugg

200 olysis bullosa (RDEB), a currently incurable blistering genodermatosis caused by loss-of-function mut

201 The development and evolution of blistering had a similar pattern in mannan-binding lecti

202 sms of continued autoantibody production and blistering have been well characterized using AIBD anima

203 ulates both autoantibody production and skin blistering in a prototypical organ-specific autoimmune d

204 ogy and suggest novel strategies to suppress blistering in bulbous impetigo and staphylococcal scalde

205 sease in C57Bl/10.s (H2s), (iii) microscopic blistering in DBA/1J (H2q), (iv) only presence of non-pa

206 n of the gene encoding RSU-1 results in wing blistering in Drosophila, demonstrating its role in inte

207 infiltrating neutrophils and the subsequent blistering in experimental BP.

208 ensate for the mutant K14 and thus ease skin blistering in K14 EBS patients, we cloned the promoter o

209 chemical sulforaphane (SF) ameliorates skin blistering in keratin 14 (K14)-deficient mice, correlati

210 of p38 MAPK phosphorylation and subepidermal blistering in MC-deficient mice.

211 tly, TP abrogated autoantibody-mediated skin blistering in mice and was effective when applied topica

212 However, recent demonstrations of skin blistering in multisystem disorders with single gene def

213 anti-BP180 IgG failed to induce subepidermal blistering in NE-null (NE(-/-)) mutant mice.

214 use IgGs from these individuals induced skin blistering in neonatal mice caused by suprabasal acantho

215 keletal reorganization in tissue culture and blistering in pemphigus mouse models.

216 Perp-/- mice die postnatally, with dramatic blistering in stratified epithelia symptomatic of compro

217 lysis bullosa simplex (EBS), a disorder with blistering in the basal layer due to cell fragility.

218 ant Dsc3, M3AR, or SPCA1 both prevented skin blistering in the passive transfer of AuAbs model of PV

219 in pemphigus vulgaris, with mucosal-dominant blistering in the suprabasal layer of the epidermis.

220 e lacking the desmosome protein Perp exhibit blistering in their stratified epithelia and display pos

221 neutrophils play a key role in subepidermal blistering in this animal model.

222 lar link between IgE autoantibodies and skin blistering in this murine model of BP.

223 APK blocked the ability of PF IgGs to induce blistering in vivo.

224 Loss of Pod1 in mice leads to epicardial blistering, increased SM differentiation on the surface

225 These results indicate that PF IgG-induced blistering is dependent on activation of p38 MAPK in the

226 ive transfer mouse model of BP, subepidermal blistering is triggered by anti-BP180 antibodies and dep

227 In experimental BP, subepidermal blistering is triggered by rabbit anti-murine BP180 (mBP

228 followed by hyperkeratosis and less frequent blistering later in life.

229 None of the 3 blistering mice examined had small-bowel pathology.

230 ntified 21 patients who developed widespread blistering mucocutaneous reactions without any suspected

231 No blistering occurred during the mean 2.2 years of follow-

232 (SEM) showed characteristics of melting and blistering of TD MPs and shredding and flaking of LS MPs

233 toimmune disease characterized by subcorneal blistering of the epidermis and the production of autoan

234 gus vulgaris (PV) is a disease that features blistering of the skin and mucous membranes caused by au

235 adherin desmoglein 3 cause potentially fatal blistering of the skin and mucous membranes.

236 is a rare autoimmune disease that results in blistering of the skin and oral cavity.

237 at by using cutting-edge technology, suction blistering offers several advantages over conventional b

238 ich show exquisite pathologic specificity in blistering only the superficial epidermis.

239 mice develop normally without signs of skin blistering or muscular dystrophy.

240 f pharmaceutical proteins is proceeding at a blistering pace.

241 90 that were sensitized to gluten developed blistering pathology similar to that seen in DH.

242 intraepidermal (pemphigus) and subepidermal blistering (pemphigoid diseases and dermatitis herpetifo

243 This junctional blistering phenocopies defects reported in newborn alpha

244 mal junction, and a complete reversal of the blistering phenomenon with the administration of a glute

245 le recombination within this region and seed-blistering phenotype could be an indication of a transpo

246 whereas the majority of Lamc2-/- mice showed blistering phenotype on days 1 to 2 and died within 5 da

247 A blistering phenotype reminiscent of the phenotype observ

248 t3 in the mutant background rescued the wing blistering phenotype, whereas expression of another fami

249 osine cross-linking activity, explaining the blistering phenotype.

250 disadhesion of keratinocytes manifested with blistering phenotype.

251 While K16 is capable of rescuing the blistering, phenotypic complementation in the resulting

252 drome in man, which is characterized by skin blistering, premature skin aging and skin cancer of unkn

253 the causative agent for severe mucocutaneous blistering reactions mimicking SCAR.

254 eralized skin fragility, trauma-induced skin blistering since infancy, and development of remarkable

255 ing, the recruitment of therapeutic cells to blistering skin and to more advanced skin lesions remain

256 e (HHD) (MIM 16960) is an autosomal-dominant blistering skin disease caused by a mutation in the Ca2+

257 Hailey-Hailey disease (MIM16960) is a blistering skin disease caused by mutations in the Ca2+

258 Dystrophic epidermolysis bullosa (DEB) is a blistering skin disease caused by mutations in the gene

259 Fogo selvagem (FS) is a blistering skin disease caused by pathogenic IgG4 autoan

260 Bullous pemphigoid is a blistering skin disease characterized by autoantibodies

261 lgaris (PV) is a life-threatening autoimmune blistering skin disease characterized by detachment of k

262 Pemphigus foliaceus is an autoimmune blistering skin disease characterized by intraepidermal

263 murine BP180 (mBP180) ectodomain triggers a blistering skin disease in mice that depends on compleme

264 The autoimmune blistering skin disease pemphigus is caused by IgG autoa

265 ced by autoantibodies from patients with the blistering skin disease pemphigus vulgaris (PV) IgG is r

266 ion is observed in the autoantibody-mediated blistering skin disease pemphigus vulgaris (PV), we appl

267 Patients with the blistering skin disease pemphigus vulgaris (PV), which i

268 dler syndrome (KS) is an autosomal recessive blistering skin disease resulting from pathogenic mutati

269 Hailey-Hailey disease (HHD) is blistering skin disease, resulting from mutations in the

270 a group of autosomal dominant and recessive blistering skin diseases in which pathogenic mutations h

271 ding of many aspects of the major autoimmune blistering skin diseases, pemphigus and bullous pemphigo

272 1 and plakogloben in staphylococcal-mediated blistering skin diseases.

273 bullous pemphigoid are autoantibody-mediated blistering skin diseases.

274 epidermolysis bullosa (RDEB) is an inherited blistering skin disorder caused by mutations in the COL7

275 The blistering skin disorder epidermolysis bullosa simplex (

276 e dystrophic epidermolysis bullosa (RDEB), a blistering skin disorder often accompanied by epidermal

277 severe inherited human diseases, such as the blistering skin disorder recessive dystrophic epidermoly

278 rmatitis herpetiformis (DH) is an autoimmune blistering skin disorder that is associated with gluten

279 rmatitis herpetiformis (DH) is an autoimmune blistering skin disorder that is associated with intesti

280 Bullous pemphigoid is a blistering skin disorder with increased mortality.

281 eficient epidermal adhesion is a hallmark of blistering skin disorders and chronic wounds, implicatin

282 kievirus A6 (CVA6) DNA was identified in the blistering skin lesions in 6 of 21 patients.

283 lammatory disease characterized by recurrent blistering skin lesions, bronchiolitis, arthralgia, ocul

284 Loss of PRC1 resulted in blistering skin, reminiscent of human skin fragility syn

285 recessive disorder characterized by neonatal blistering, sun sensitivity, atrophy, abnormal pigmentat

286 4) and in women who experienced at least one blistering sunburn (hazard ratio = 2.17, 95% confidence

287 r ability to achieve a tan, and history of a blistering sunburn were associated with a higher risk of

288 ll as height, hours spent in the summer sun, blistering sunburns during adolescence, and moles, all i

289 The lifetime number of blistering sunburns was also positively associated with

290 escent, and higher lifetime number of severe/blistering sunburns.

291 thenia gravis, Guillain-Barre syndrome, skin blistering syndromes, and Kawasaki disease.

292 , RDEB individuals manifest unremitting skin blistering that evolves into chronic wounds, inflammatio

293 With regard to skin blistering, the clinicopathological findings expand the

294 in fragility characterized by intraepidermal blistering upon mild mechanical trauma.

295 n PV, but may function downstream to augment blistering via Dsg3 endocytosis.

296 ntified rod domain hotspots and the severest blistering was associated with mutations in the helix bo

297 s between blister and biopsy AD, but suction blistering was superior in cell-specific resolution for

298 ies, the proband was a newborn with neonatal blistering with no evidence for muscle weakness as yet.

299 A biopsy specimen showed subepidermal blistering with prominent inflammatory cells, including

300 ous disorder characterized by intraepidermal blistering within the basal keratinocytes as a result of