ライフサイエンスコーパス: blistering

1 bsequent MC degranulation, and ultimately BP blistering.

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

3 lustrated in a patient with mucosal-dominant blistering.

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

5 epidermal cell detachment (acantholysis) and blistering.

6 ak of p38MAPK activation but failed to block blistering.

7 rmolysis bullosa simplex with intraepidermal blistering.

8 desmoglein-1-specific autoantibodies induce blistering.

9 rized by oral mucosal erosions and epidermal blistering.

10 immune disease characterized by subepidermal blistering.

11 tinocytes leading to epidermal cytolysis and blistering.

12 ing in severe mucosal erosions and epidermal blistering.

13 culating pathogenic IgG levels and prevented blistering.

14 hil infiltration and subsequent subepidermal blistering.

15 thereby moderating the severity of the skin blistering.

16 y, because mutations in k10 lead to abnormal blistering.

17 f K14 developed normally without evidence of blistering.

18 wing surface apposition and consequent wing blistering.

19 to induce painful cutaneous inflammation and blistering.

20 late onset of mild skin fragility and acral blistering.

21 icantly reduced PAO-induced inflammation and blistering.

22 rsenicals-induced cutaneous inflammation and blistering.

23 3) IgG autoantibodies cause life-threatening blistering.

24 prophylactic IL-1ra administration prevented blistering.

25 adjunctive therapy for control of pemphigus blistering.

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

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

28 dermis of wounds, characterized by extensive blistering.

29 -mediated inhibition of DSG3 binding to skin blistering.

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

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

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

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

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 The patient was born with extensive blistering and demonstrated negative immunofluorescence

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

40 form erythroderma (BCIE) is characterized by blistering and erythroderma in infancy and by erythroder

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Clinically, there was generalized blistering but only mild scarring.

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

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

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

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

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

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

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

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

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

75 246D and D392N) responsible for a C. elegans blistering cuticle phenotype was also investigated.

76 Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody

77 the skin in gelatinase B-deficient mice, but blistering did not occur.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 emphigoid (BP) is an autoimmune subepidermal blistering disease characterized by deposition of autoan

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

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

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

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

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

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

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

112 urine BP180 are known to trigger a cutaneous blistering disease in mice by passive transfer experimen

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 s vulgaris (PV) is an Ab-mediated autoimmune blistering disease of mucotaneous surfaces.

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

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

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

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

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

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

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

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

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

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

131 bullosa (JEB) is an autosomal recessive skin blistering disease with both lethal and nonlethal forms,

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

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

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

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

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

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

138 ) is a chronic mucocutaneous autoimmune skin blistering disease.

139 a potentially fatal autoimmune mucocutaneous blistering disease.

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

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

142 a potentially fatal autoimmune mucocutaneous blistering disease.

143 ents with this potentially lethal autoimmune blistering disease.

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

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

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

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

148 Autoimmune blistering diseases are a heterogeneous group of about a

149 Autoimmune blistering diseases are characterized by substantial mor

150 Autoimmune blistering diseases are generally distinct entities char

151 In the blistering diseases bullous impetigo and staphylococcal

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

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

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

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

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

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

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

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

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

161 d bullous pemphigoid are distinct autoimmune blistering diseases that are characterised by the presen

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

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

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

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

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

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

168 ntinents dedicating their work to autoimmune blistering diseases.

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

170 Pemphigus is an autoimmune blistering disorder associated with significant morbidit

171 dermal integrity is evident in the inherited blistering disorder associated with the absence of a fun

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

173 MIM#226700) is a lethal, autosomal recessive blistering disorder caused by mutations in one of the th

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

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

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

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

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

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

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

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

182 enetically heterogeneous autosomal recessive blistering disorder, including lethal and nonlethal vari

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

184 The blistering disorder, lethal junctional epidermolysis bul

185 thologic diagnosis of an acquired autoimmune blistering disorder.

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

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

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

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

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

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

192 psoriasis, allergic contact dermatitis, and blistering disorders.

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

194 effective for treating desmosome autoimmune blistering disorders.

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

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

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

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

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 56 in the wing imaginal disc results in wing blistering in adults, a phenotype also observed with bot

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

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

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

208 infiltrating neutrophils and the subsequent blistering in experimental BP.

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

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

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

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

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

214 cantholysis of human foreskin in culture and blistering in neonatal mice.

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

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

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

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

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

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

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

225 erimental BP model in mice, the subepidermal blistering is mediated by antibodies directed against th

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 er characterized by epidermal thickening and blistering, is caused by mutations in the late-different

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

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

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

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

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

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

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

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

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

238 wing fail to connect properly, resulting in 'blistering' of the wing and the formation of extra cross

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

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

241 f pharmaceutical proteins is proceeding at a blistering pace.

242 90 that were sensitized to gluten developed blistering pathology similar to that seen in DH.

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

244 This junctional blistering phenocopies defects reported in newborn alpha

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

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

247 ssing a control K16-C14 cDNA also rescue the blistering phenotype of the K14 null mice with only a sm

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

249 A blistering phenotype reminiscent of the phenotype observ

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

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

252 disadhesion of keratinocytes manifested with blistering phenotype.

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

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

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

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

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

258 toantibodies in the serum of patients with a blistering skin disease called bullous pemphigoid (BP),

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

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

261 Bullous pemphigoid is a blistering skin disease characterized by autoantibodies

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

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

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

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

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

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

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

269 VII collagen gene, COL7A1, give rise to the blistering skin disease, dystrophic epidermolysis bullos

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

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

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 tegrity, since their absence gives rise to a blistering skin disorder in neonatal epidermis, and hemo

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

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

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

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

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

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

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

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

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 ation codon mutation, may explain the milder blistering tendency of the skin in this patient.

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

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

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

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

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

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