ライフサイエンスコーパス: blister

1 induces cutaneous erythema, edema and micro-blisters.

2 s to type VII collagen causing mucocutaneous blisters.

3 ing to clinical and histologic resolution of blisters.

4 uman COL7 transgene and induced subepidermal blisters.

5 goid have been reported to have itch without blisters.

6 ude mice neither produced autoantibodies nor blisters.

7 e period delayed autoantibody production and blisters.

8 findings of bullous pemphigoid, itch, and no blisters.

9 times associated with erythema, pruritus and blisters.

10 underlying pathophysiology of inherited skin blistering.

11 to induce painful cutaneous inflammation and blistering.

12 late onset of mild skin fragility and acral blistering.

13 icantly reduced PAO-induced inflammation and blistering.

14 rsenicals-induced cutaneous inflammation and blistering.

15 3) IgG autoantibodies cause life-threatening blistering.

16 prophylactic IL-1ra administration prevented blistering.

17 adjunctive therapy for control of pemphigus blistering.

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

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

20 dermis of wounds, characterized by extensive blistering.

21 -mediated inhibition of DSG3 binding to skin blistering.

22 bsequent MC degranulation, and ultimately BP blistering.

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

24 Ab could prevent keratinocyte detachment and blistering.

25 rmolysis bullosa simplex with intraepidermal blistering.

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

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

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

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

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

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

32 rofiles of key inflammatory pathways between blister and biopsy AD, but suction blistering was superi

33 in the epidermis, however, resulted in skin blister and hair follicle phenotypes that were considera

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

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

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

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

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

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

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

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

42 cations in Puget Sound and examined them for blisters and burrows caused by polychaete worms.

43 ectron microscopy revealed that the nitrated blisters and edge-like carbon structures, enabling highl

44 oped an acute eruption of oral and cutaneous blisters and erosions 2 days after receiving a diphtheri

45 antibodies are related to the occurrence of blisters and erosions may encourage further studies on t

46 pidermal keratinocyte adhesion, resulting in blisters and erosions of the skin and mucous membranes.

47 epidermal junction and, clinically, by tense blisters and erosions on skin or mucous membranes close

48 elong generalized trauma-induced spontaneous blisters and erosions, particularly around the ankles.

49 Cellular infiltrate was isolated by suction blisters and examined by flow cytometry.

50 nti-BP180 IgG failed to develop subepidermal blisters and exhibited a drastic reduction in p38 MAPK p

51 cts and secretory portions were dilated, and blisters and papules formed on the skin surface in the k

52 Formation of water blisters and phase separation at the adhesive/dentin int

53 mi-lethality; adult survivors developed wing blisters and were flightless due to a lack of intercellu

54 int pain, joint swelling, vesicular lesions (blisters), and rashes from days 1 to 42.

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

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

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

58 bly of defects such as scars, pleats, folds, blisters, and liquid crystal ripples.

59 reatening autoimmune skin disease, epidermal blisters are caused by autoantibodies primarily targetin

60 While fever blisters are more common, occasionally the cornea is inf

61 r wild-type littermates, do not develop skin blisters, are fertile, and survive >1.5 years.

62 n, who develop symptoms ranging from painful blisters around their mouths and hands to neurological c

63 mutant neutrophils emigrating into a suction blister at 16 hours was the same as the percentage in pe

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

65 e of STAT3 mutant neutrophils migrating into blisters at 16 hours was the same as in peripheral blood

66 ular recruitment in cantharidin-induced skin blisters at 24 and 72 hours.

67 83 (74%) of 112 patients had three or fewer blisters at 6 weeks compared with 92 (91%) of 101 patien

68 oportion of participants with three or fewer blisters at 6 weeks.

69 tromal cells, some of which localised to the blisters at the epidermal-dermal boundary.

70 dults with bullous pemphigoid (three or more blisters at two or more sites and linear basement membra

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

72 mall molecule produced by several species of blister beetle.

73 arwinylus marcosi, family Oedemeridae (false blister beetles), that had an earlier gymnosperm (most l

74 ementary DNA library from leaf tissue of the blister blight-resistant tea cultivar TRI2043 and functi

75 independent of the targeted epitopes, induce blisters both ex vivo and in vivo.

76 t the single Drosophila SRF ortholog, termed Blistered (Bs), is expressed in all adult muscles, but B

77 hibit spontaneous but not induced suprabasal blisters by PV mAbs in mouse passive transfer models.

78 Suction blistering captured epidermal and most immune cells equa

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

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

81 K2 is also activated in human pemphigus skin blisters, causing translocation of MK2 from the nucleus

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

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

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

85 atment with oral prednisolone for short-term blister control in bullous pemphigoid and significantly

86 with doxycycline gives acceptable short-term blister control while conferring long-term safety advant

87 hat interlayer shearing and sliding near the blister crack tip, caused by the transition from membran

88 pyrolytic graphite, utilizing atomic-scale 'blisters' created in the top layer by neon atom intercal

89 246D and D392N) responsible for a C. elegans blistering cuticle phenotype was also investigated.

90 Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody

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

92 ation of keratinocyte cell-cell adhesion and blister development.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 ents with this potentially lethal autoimmune blistering disease.

126 ) is a chronic mucocutaneous autoimmune skin blistering disease.

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

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

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

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

131 Autoimmune blistering diseases are a heterogeneous group of about a

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

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

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

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

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

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

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

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

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

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

142 ntinents dedicating their work to autoimmune blistering diseases.

143 Pemphigus is an autoimmune blistering disorder associated with significant morbidit

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

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

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

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

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

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

150 thologic diagnosis of an acquired autoimmune blistering disorder.

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

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

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

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

155 psoriasis, allergic contact dermatitis, and blistering disorders.

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

157 Whole-genome microarray analysis of suction-blister epidermis obtained throughout the day revealed a

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

159 dSRF (Blistered) expression in specific regions of the larval

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

161 biopsy specimens (n = 16), serum (n = 114), blister fluid (n = 23), and primary inflammatory cells f

162 CXCL10 levels were higher in blister fluid (P < .0001) and serum (P < .005) from pati

163 groups when using either serum (P < 0.05) or blister fluid (P < 0.001) specimens from BP patients.

164 ISA (P-ELISA) system, only 2 muL of serum or blister fluid and 70 min were required to detect anti-NC

165 ereas similarities between lipid profiles in blister fluid and epidermis indicated a primarily epider

166 ling lipid mediators in biopsies and suction blister fluid can support studies investigating cutaneou

167 13) among the top upregulated proteins in AD blister fluid proteomic analyses.

168 ocesses associated with disease progression, blister fluid, serum, and biopsy specimens were collecte

169 ated a primarily epidermal origin of suction blister fluid.

170 ids, in human dermis, epidermis, and suction blister fluid.

171 f mainly CD15(+) neutrophils was observed in blister fluid.

172 lso showed that abundance of CXCR2 ligand in blister fluids also creates a favorable milieu for the r

173 CVA6 viral particles were identified in the blister fluids and skin lesions by electron microscopy.

174 Blister fluids displayed high levels of IL-6, IL-17, IL-

175 Both sera and/or blister fluids from 14 untreated BP patients were analyz

176 ere, we analyzed cytokines and chemokines in blister fluids of patients affected by dystrophic, junct

177 and CCR2(+) myeloid cells toward EB-derived blister fluids.

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

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

180 ed by baseline severity (3-9, 10-30, and >30 blisters for mild, moderate, and severe disease, respect

181 pathogenesis of BP with a specific focus on blister formation and to define conditions inducing derm

182 ymerase-chain-reaction assay, and documented blister formation and wound healing with the use of digi

183 e investigated dominant modification of wing blister formation caused by knock-down of eogt.

184 se of the skin characterized by subepidermal blister formation due to tissue-bound and circulating au

185 ound abundantly in BP lesions, their role in blister formation has remained unclear.

186 e necessary for IgE autoantibody-mediated BP blister formation in a humanized IgE receptor mouse mode

187 mechanisms leading to cell dissociation and blister formation in response to autoantibody binding.

188 ly, inhibiting EGFR prevented PV IgG-induced blister formation in the passive transfer mouse model of

189 ivated eosinophils directly contribute to BP blister formation in the presence of BP autoantibodies.

190 It is controversial whether blister formation is due to direct inhibition of Dsg, in

191 MK2-dependent and -independent mechanisms of blister formation using passive transfer of human anti-D

192 characterized by mucocutaneous fragility and blister formation, inducible by often minimal trauma.

193 lity disorder characterized by injury-driven blister formation, progressive soft-tissue fibrosis, and

194 astase expression, two proteases involved in blister formation, thereof further demonstrating its rol

195 pyrimidine synthesis alleles suppressed wing blister formation, while removal of uracil catabolism al

196 e is targeted towards minimizing the risk of blister formation, wound care, symptom relief and specif

197 e dermal-epidermal junction with no signs of blister formation.

198 neutrophil granulocytes, a precondition for blister formation.

199 in an inflammatory response and subepidermal blister formation.

200 ytosolic uracil levels, thereby causing wing blister formation.

201 ical Notch signaling pathway suppressed wing blister formation.

202 ne of affected skin, thereby contributing to blister formation.

203 aration, improved wound closure, and reduced blister formation.

204 Fluids from suction blisters formed on top of LPRs induced by using intrader

205 hat Polydora websteri are present in the mud blisters from oysters grown in Puget Sound, constituting

206 s in gene expression compared with unexposed blisters, further underscoring the relatively muted resp

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

208 Fifteen patients with itch without blisters had immunopathologic findings of bullous pemphi

209 volume in both sexes; however, at 72 hours, blisters had only resolved in females.

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

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

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

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

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

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

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

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

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

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

220 es of responders to cantharidin-induced skin blisters in male healthy volunteers: those with immediat

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

222 complement activation is a prerequisite for blister induction, this lack of function compared with I

223 stress, demonstrating that splitting at the blister interface in patient tissue is due to compromise

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

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

226 ) in early resolvers using aspirin increased blister leukocyte ALX but reduced cytokines/chemokines a

227 ised generalized scale-crusts and occasional blisters, mostly induced by trauma, as well as mild diff

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

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

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

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

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

233 d IL-18 levels in plasma and in induced skin blisters of DENV-infected patients, as well as concomita

234 state of all major leukocytes was lower, in blisters of females.

235 At 24 hours, cantharidin formed blisters of similar volume in both sexes; however, at 72

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

237 Predominance of blisters on hands and feet may be a clinical clue to the

238 n clinical features with predominantly tense blisters on hands and feet, resembling dyshidrosiform pe

239 ic infections to those with a mild fever and blisters on infected individuals' hands, feet, and throa

240 ous dermatoses (AIBD), autoantibodies induce blisters on skin or mucous membranes, or both.

241 Recent findings of mud blisters on the shells of Pacific oysters (Crassostrea g

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

243 The blister packages seem difficult to miniaturize and none

244 lear quadrupole resonance (NQR) signals from blister packs of medicines has been compared.

245 EAT) for 12 weeks administered in electronic blister packs.

246 ary: adherence, measured by using electronic blister packs.

247 EAT) for 12 weeks administered in electronic blister-packs.

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

249 This junctional blistering phenocopies defects reported in newborn alpha

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

251 sociated with the occurrence of erosions and blisters (r = 0.985; P = .006) but not urticarial and er

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

253 pal pathogen of P. lambertiana is white pine blister rust (Cronartium ribicola J.C. Fischer ex Raben.

254 in pine beetle and the non-native white pine blister rust (WPBR).

255 and mortality from the non-native white pine blister rust caused byCronartium ribicola.

256 Newly discovered associations for white pine blister rust quantitative disease resistance included 45

257 with quantitative and qualitative white pine blister rust resistance in sugar pine.

258 d fibulin-2-null mice display perinatal skin blisters similar to those in alpha3beta1-deficient mice.

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

260 Desmosomes at blister sites were occasionally split, with PV IgG decor

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

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

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

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

270 bullous pemphigoid are autoantibody-mediated blistering skin diseases.

271 1 and plakogloben in staphylococcal-mediated blistering skin diseases.

272 The blistering skin disorder epidermolysis bullosa simplex (

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

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

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

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

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

278 c and capillary valves pneumatic pumping and blister storage packages.

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

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

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

282 A pressurized blister test and mechanical resonance are used to measur

283 Here we use a pressurized blister test to directly measure the adhesion energy of

284 Results from the circular blister test, however, display seemingly anomalous behav

285 ated upon different joining mechanisms using blister tests.

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

287 into bivalve shells, creating unsightly mud blisters that are unappealing to consumers and, when nic

288 croarray examination of ex vivo LC from skin blisters that were exposed to live L3 also showed few si

289 rnal gas pressure can become great enough to blister the oxide layer.

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

291 higus foliaceus and pemphigus vulgaris cause blisters through loss of desmosomal adhesion.

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

293 rolonged sun exposure (for painful burn with blisters vs. practically no reaction, multivariable-adju

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

295 the identity of the polychaete causing these blisters, we obtained Pacific oysters from two locations

296 mouse strains developed autoantibodies, but blisters were exclusively observed in mice carrying H2s.

297 Suction blisters were induced in 1 subject, and exudate fluid wa

298 e dermal side of salt-split skin and induced blisters when transferred into healthy mice.

299 Increase occurrence of a blistered wing phenotype was found in a subset of PAMAM-

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