ライフサイエンスコーパス: pemphigus

1 ship between p38MAPK and DSG3 endocytosis in pemphigus.

2 mechanisms for the loss of cell adhesion in pemphigus.

3 sts are effective for treating patients with pemphigus.

4 bility of specific autoantibody targeting in pemphigus.

5 ens or may even have been another species of Pemphigus.

6 ittle is known about the inpatient burden of pemphigus.

7 anus or lichenoid mucositis (LP), and one as pemphigus.

8 utoimmune blistering disease, paraneoplastic pemphigus.

9 were all associated with hospitalization for pemphigus.

10 acantholysis in the neonatal mouse model of pemphigus.

11 ments possibly underlying the paraneoplastic pemphigus.

12 goid; and 1 suspected case of paraneoplastic pemphigus.

13 tions by Trichosporon inkin in patients with pemphigus.

14 oor outcome in patients with severe forms of pemphigus.

15 m infection, was detected in 2 patients with pemphigus.

16 s an effective and safe treatment option for pemphigus.

17 icacious and well tolerated in patients with pemphigus.

18 rs, and chimeric antigen receptor T cells in pemphigus.

19 tibodies in skin blistering diseases such as pemphigus.

20 t EGFR is a potential therapeutic target for pemphigus.

21 to keratinocyte (KC) detachment and death in pemphigus.

22 investigating the use of EGFR inhibitors in pemphigus.

23 ation in the passive transfer mouse model of pemphigus.

24 irus infection, fixed drug eruption, and IgA pemphigus.

25 fluorescence were negative, excluding an IgA pemphigus.

26 rheumatoid arthritis, bronchial asthma (6%), pemphigus (5%), or other processes (9%).

27 years for those with a primary diagnosis of pemphigus; 70.6 [0.32] years for those with a secondary

28 and a consequence of, p38MAPK activation in pemphigus acantholysis.

29 matrix (eg, pemphigoid) or cell-to-cell (eg, pemphigus) adhesion in skin.

30 Pemphigus and bullous pemphigoid are autoantibody-mediat

31 Pemphigus and bullous pemphigoid are distinct autoimmune

32 tion for all the diseases studied except for pemphigus and linear immunoglobulin A disease.

33 Various experimental mouse models of pemphigus and pemphigoid disease are increasingly being

34 The Pathogenesis of Pemphigus and Pemphigoid Meeting, organized by the Depar

35 herapeutic efficacy of HDIG treatment in the pemphigus and pemphigoid models is dependent on FcRn.

36 rs that are characterized by intraepidermal (pemphigus) and subepidermal blistering (pemphigoid disea

37 with bullous pemphigoid (BP), none of 7 with pemphigus, and 3 of 32 other controls.

38 ears for those with a secondary diagnosis of pemphigus; and 47.9 [0.19] years for those without a dia

39 Although it is accepted that pemphigus antibody binding to keratinocytes (KCs) evokes

40 antigens have been cloned and characterized; pemphigus antigens are desmogleins (cell adhesion molecu

41 iated diseases, patients with paraneoplastic pemphigus, as well as patients with pemphigus vulgaris a

42 controversial findings about the effects of pemphigus autoantibodies and other inflammatory mediator

43 These studies suggest that pemphigus autoantibodies inhibit the adhesive function o

44 ssical cadherins as immunological targets of pemphigus autoantibodies is unknown.

45 s may be linked to a common pathway by which pemphigus autoantibodies lead to acantholysis.

46 ratified squamous epithelia and suggest that pemphigus autoantibodies might interfere directly with s

47 determine the epitopes and pathogenicity of pemphigus autoantibodies.

48 ameliorated loss of cell adhesion induced by pemphigus autoantibodies.

49 n because RhoA activation was shown to block pemphigus autoantibody-induced cell dissociation.

50 The mechanism responsible for pemphigus autoantibody-induced epidermal injury is not f

51 a valuable adjunctive therapy for control of pemphigus blistering.

52 Pemphigus bursarius is a host-alternating aphid in which

53 as well as resistance to lettuce root aphid (Pemphigus bursarius L.), Ra, are encoded by RGC2 family

54 used to examine the population structure of Pemphigus bursarius, a cyclically parthenogenetic aphid.

55 ects in anti-desmocollin and anti-desmoglein pemphigus, despite their identical clinical presentation

56 Recently, the clinical pemphigus disease activity indexes of Pemphigus Disease

57 ntibodies are known to correlate mostly with pemphigus disease activity.

58 inical pemphigus disease activity indexes of Pemphigus Disease Area Index (PDAI), Autoimmune Bullous

59 0.69; P = .009) and low correlation with the Pemphigus Disease Area Index (R = 0.42) and Autoimmune B

60 ir 50s, 60s, or 70s with pemphigus vulgaris (Pemphigus Disease Area Index score, 15-84 at diagnosis)

61 ability and convergent validity of the PDAI (pemphigus disease area index).

62 Pemphigus encompasses a group of autoimmune blistering d

63 The pemphigus family of autoimmune bullous disorders is char

64 In this group, there is an endemic form of pemphigus foliaceus (also known as fogo selvagem [FS]) i

65 serum samples from 60 patients with endemic pemphigus foliaceus (fogo selvagem) who lived in Limao V

66 Pemphigus foliaceus (PF) and pemphigus vulgaris (PV) are

67 Pemphigus foliaceus (PF) and the endemic form Fogo Selva

68 Patients with pemphigus foliaceus (PF) have blisters on skin, but not

69 Pemphigus foliaceus (PF) is a blistering disease caused

70 Pemphigus foliaceus (PF) is a human autoimmune blisterin

71 Pemphigus foliaceus (PF) is an antibody-mediated autoimm

72 Pemphigus foliaceus (PF) is an autoimmune skin blisterin

73 Pemphigus foliaceus (PF) is an organ-specific autoimmune

74 Fogo selvagem (FS) and pemphigus foliaceus (PF) possess pathogenic IgG anti-des

75 er murine models of bullous pemphigoid (BP), pemphigus foliaceus (PF), and pemphigus vulgaris (PV) to

76 In pemphigus vulgaris and pemphigus foliaceus (PF), autoantibodies against desmogl

77 In pemphigus foliaceus (PF), autoantibodies against desmogl

78 Fogo selvagem (FS), the endemic form of pemphigus foliaceus (PF), is an autoimmune blistering di

79 Fogo selvagem (FS), the endemic form of pemphigus foliaceus (PF), is characterized by pathogenic

80 The anti-desmoglein 1 antibodies in pemphigus foliaceus and anti-desmoglein 3 antibodies in

81 sults suggest that a subset of patients with pemphigus foliaceus and fogo selvagem have antibodies to

82 ntibodies to desmoglein-3 from patients with pemphigus foliaceus and fogo selvagem induced a pemphigu

83 s to desmoglein-3 in 19 of 276 patients with pemphigus foliaceus and fogo selvagem, who had cutaneous

84 antibodies to desmoglein-3 in patients with pemphigus foliaceus and fogo selvagem.

85 After passive transfer of pemphigus foliaceus and pemphigus vulgaris immunoglobuli

86 not necessary for blister formation, because pemphigus foliaceus and pemphigus vulgaris immunoglobuli

87 Pemphigus foliaceus and pemphigus vulgaris immunoglobuli

88 Pemphigus vulgaris and pemphigus foliaceus are cutaneous autoimmune diseases ch

89 The autoantigens for pemphigus vulgaris and pemphigus foliaceus are desmoglein 3 and desmoglein 1, r

90 Pemphigus vulgaris and pemphigus foliaceus are two closely related, but clinica

91 ntigens recognized by pemphigus vulgaris and pemphigus foliaceus autoantibodies are desmoglein-3 (Dsg

92 th pemphigus vulgaris and five patients with pemphigus foliaceus by nested polymerase chain reaction

93 An elderly man with pemphigus foliaceus died despite treatment with liposoma

94 ring diseases such as pemphigus vulgaris and pemphigus foliaceus have non-cell-intrinsic bases.

95 phenotype in skin organ cultures and because pemphigus foliaceus IgGs produce a distinct phenotype in

96 nd the clinical onset of the endemic form of pemphigus foliaceus in a Brazilian community with a high

97 Endemic pemphigus foliaceus in humans, known as Fogo Selvagem (F

98 Pemphigus foliaceus is an autoimmune blistering skin dis

99 Pemphigus foliaceus is an autoimmune skin disease mediat

100 bodies in pemphigus vulgaris induced typical pemphigus foliaceus lesions in neonatal mice, whereas th

101 lein 1 specific T cell clones generated from pemphigus foliaceus patients by clonal expansion in vitr

102 e and after clinical disease and 60 Japanese pemphigus foliaceus patients.

103 the T cell receptor of T cells derived from pemphigus foliaceus patients.

104 , and 30 controls with pemphigus vulgaris or pemphigus foliaceus were included for comparison.

105 here in Brazil, 372 normal subjects (without pemphigus foliaceus) from Limao Verde and surrounding lo

106 patients (pemphigus vulgaris, 84 [91%], and pemphigus foliaceus, 8 [9%]) who received rituximab trea

107 In pemphigus foliaceus, and its endemic form, fogo selvagem

108 n the pathogenesis of pemphigus vulgaris and pemphigus foliaceus, including its endemic form fogo sel

109 Fogo selvagem (FS), the endemic form of pemphigus foliaceus, is a cutaneous autoimmune disease c

110 Endemic pemphigus foliaceus, like the sporadic form seen in the

111 well as patients with pemphigus vulgaris and pemphigus foliaceus, were studied.

112 patients with pemphigus vulgaris and 2 with pemphigus foliaceus.

113 blister formation in pemphigus vulgaris and pemphigus foliaceus.

114 on of epidermal cells to each other (eg, the pemphigus group of disorders).

115 Paraneoplastic pemphigus has been associated with both malignancies and

116 To determine whether individuals without pemphigus have B cell tolerance to Dsg1, we cloned mAbs

117 Using passive transfer of pemphigus IgG to normal and DSG3(null) neonatal mice, we

118 Inhibition of p38MAPK blocked pemphigus IgG-induced cytoskeletal reorganization in tis

119 rp in desmosome assembly and trafficking and pemphigus IgG-mediated acantholysis, providing further i

120 ays is emerging as an important component of pemphigus IgG-mediated acantholysis.

121 important role in the ability of pathogenic pemphigus IgGs to induce blistering and that both p38 mi

122 t plasminogen activator is not necessary for pemphigus immunoglobulin G to induce acantholysis in the

123 blister formation, we passively transferred pemphigus immunoglobulin G to urokinase plasminogen acti

124 tivator does not inhibit blisters induced by pemphigus immunoglobulin G.

125 There is a significant inpatient burden for pemphigus in the United States.

126 in sera from 24 patients with paraneoplastic pemphigus (including 10 with concomitant Castleman's dis

127 are for patients with a primary diagnosis of pemphigus increased significantly from 2002 to 2012 (ana

128 Pemphigus is a life-threatening autoimmune disease in wh

129 Pemphigus is a life-threatening blistering disorder of t

130 Pemphigus is a rare autoimmune disease that results in b

131 Pemphigus is an autoimmune blistering disorder associate

132 Pemphigus is an autoimmune disease of skin adhesion asso

133 The autoimmune blistering skin disease pemphigus is caused by IgG autoantibodies against desmos

134 performing multicenter controlled trials for pemphigus is the lack of a validated disease activity sc

135 nce its contribution to cell dissociation in pemphigus is well established.

136 In pemphigus, keratinocytes in epidermis and mucous membran

137 diagnoses of pemphigus vulgaris and clinical pemphigus lesions (mean [SD] age, 43.3 [1.7] years; age

138 Pemphigus lesions are mediated directly by the autoantib

139 levated tissue-type plasminogen activator in pemphigus lesions.

140 monolayers with anti-alpha9 antibody induced pemphigus-like acantholysis, which could be reversed eit

141 yte protein band both stained epidermis in a pemphigus-like pattern and induced acantholysis in kerat

142 Detailed characterization of these pemphigus mAbs should lead to a better understanding of

143 leda, vitiligo, palmoplantar pustulosis, and pemphigus may be mediated, in part, by the non-neuronal

144 nization in tissue culture and blistering in pemphigus mouse models.

145 (BSLE) (n = 3), bullous pemphigoid (n = 16), pemphigus (n = 11), and normal controls (n = 12).

146 dwelling colonies of a social aphid species (Pemphigus obesinymphae) are not pure clones, but are inv

147 Only the presence of pemphigus or liver dysfunction correlated with a bad pro

148 Familial benign pemphigus, or Hailey-Hailey disease (HHD), is a rare and

149 ajority of laboratories currently working on pemphigus pathogenesis, it aims to serve as a solid basi

150 filament retraction, which are hallmarks of pemphigus pathogenesis, TP may serve as a promising trea

151 t S2849 represents an important mechanism in pemphigus pathogenesis, which, by reversing Ca(2+) insen

152 the relevance of the apoptotic mechanism in pemphigus pathogenesis.

153 are blocked by autoantibodies from multiple pemphigus patients.

154 histologically similar to those observed in pemphigus patients.

155 n and mucocutaneous acantholysis observed in pemphigus patients.

156 eir native environment and uncommon in other pemphigus phenotypes and in FS patients who migrate to u

157 autoimmune diseases of the skin such as the pemphigus phenotypes and others.

158 Sera of patients with paraneoplastic pemphigus (PNP) characteristically immunoprecipitate fiv

159 ted with a primary or secondary diagnosis of pemphigus, respectively; when factoring in weights that

160 us, the anti-desmoglein antibody profiles in pemphigus sera and the normal tissue distributions of Ds

161 adherin IgG autoantibodies detected in these pemphigus sera remains to be defined.

162 ls (E-cadherin positive, Dsg1 negative) with pemphigus sera showed negative results.

163 SA, anti-E-cadherin IgG was detected in most pemphigus sera that produced strong E-cadherin bands by

164 MK2 is also activated in human pemphigus skin blisters, causing translocation of MK2 fr

165 and health care disparities with respect to pemphigus, such that poor, nonwhite, and/or uninsured or

166 nstrating two peaks of p38MAPK activation in pemphigus tissue culture and mouse models.

167 of 10 dermatologists scored 15 patients with pemphigus to estimate the inter- and intra-rater reliabi

168 of HHV8 infection was found in all types of pemphigus using a variety of methods.

169 Pemphigus vulgaris (n=40, USA and Japan), bullous pemphi

170 Five women in their 50s, 60s, or 70s with pemphigus vulgaris (Pemphigus Disease Area Index score,

171 Pemphigus foliaceus (PF) and pemphigus vulgaris (PV) are autoimmune blistering diseas

172 ients with the immunoblistering skin disease pemphigus vulgaris (PV) can induce keratinocyte (KC) dys

173 not mucous membranes, whereas patients with pemphigus vulgaris (PV) develop blisters on mucous membr

174 Pemphigus vulgaris (PV) encompasses two clinical phenoty

175 Patients with pemphigus vulgaris (PV) harbor antibodies reactive again

176 The development of nonhormonal treatment of pemphigus vulgaris (PV) has been hampered by a lack of c

177 om patients with the blistering skin disease pemphigus vulgaris (PV) IgG is reduced in maturated desm

178 t EGF receptor (EGFR) is activated following pemphigus vulgaris (PV) IgG treatment of primary human k

179 Because pemphigus vulgaris (PV) IgGs adsorbed on the rDsg3-Ig-Hi

180 Pemphigus vulgaris (PV) is a cutaneous autoimmune diseas

181 IMPORTANCE Pemphigus vulgaris (PV) is a disease that features blist

182 Pemphigus vulgaris (PV) is a life-long, potentially fata

183 Pemphigus vulgaris (PV) is a life-threatening autoimmune

184 Pemphigus vulgaris (PV) is a life-threatening autoimmune

185 Pemphigus vulgaris (PV) is a life-threatening autoimmune

186 Pemphigus vulgaris (PV) is a potentially fatal autoimmun

187 Pemphigus vulgaris (PV) is a potentially fatal autoimmun

188 Pemphigus vulgaris (PV) is a potentially fatal blisterin

189 Pemphigus vulgaris (PV) is a potentially fatal blisterin

190 Pemphigus vulgaris (PV) is a potentially fatal blisterin

191 Pemphigus vulgaris (PV) is a potentially lethal mucocuta

192 Pemphigus vulgaris (PV) is a prototypic tissue-specific

193 Pemphigus vulgaris (PV) is an Ab-mediated autoimmune bli

194 Pemphigus vulgaris (PV) is an autoimmune blistering dise

195 Pemphigus vulgaris (PV) is an autoimmune blistering dise

196 Pemphigus vulgaris (PV) is an autoimmune blistering dise

197 Pemphigus vulgaris (PV) is an autoimmune blistering dise

198 Pemphigus vulgaris (PV) is an autoimmune bullous disease

199 Pemphigus vulgaris (PV) is an autoimmune disease mediate

200 Pemphigus vulgaris (PV) is an autoimmune disorder in whi

201 Pemphigus vulgaris (PV) is an autoimmune epidermal blist

202 Pemphigus vulgaris (PV) is an epidermal blistering disor

203 Pemphigus vulgaris (PV) is considered as a model for an

204 Pemphigus vulgaris (PV) is mediated by autoantibodies to

205 In the human autoimmune blistering disease pemphigus vulgaris (PV) pathogenic antibodies bind the d

206 A loss of epidermal cohesion in pemphigus vulgaris (PV) results from autoantibody action

207 re responsible for blisters in patients with pemphigus vulgaris (PV) stems from the ability of rDsg1

208 mphigoid (BP), pemphigus foliaceus (PF), and pemphigus vulgaris (PV) to test the hypothesis that the

209 0 antibody rituximab is highly effective for pemphigus vulgaris (PV) treatment.

210 esmoglein 3 (Dsg3) in the autoimmune disease pemphigus vulgaris (PV), as well as B cells responding t

211 In the autoimmune skin-blistering disease pemphigus vulgaris (PV), autoantibodies (IgG) target the

212 In patients with pemphigus vulgaris (PV), autoantibodies against desmogle

213 in the antibody-mediated autoimmune disease pemphigus vulgaris (PV), autoantigen-based chimeric immu

214 ealth is evidenced by the autoimmune disease pemphigus vulgaris (PV), in which autoantibodies against

215 utoantibody-mediated blistering skin disease pemphigus vulgaris (PV), we applied antibody fractions o

216 There are two major clinical subsets of pemphigus vulgaris (PV)-mucosal PV (mPV) and mucocutaneo

217 s Skin Disorder Intensity Score (ABSIS), and Pemphigus Vulgaris Activity Score (PVAS) were validated

218 but it mediates tissue damage in autoimmune pemphigus vulgaris and "IgG4-related disease." Approxima

219 cloned by phage display from 3 patients with pemphigus vulgaris and 2 with pemphigus foliaceus.

220 hundred patients with confirmed diagnoses of pemphigus vulgaris and clinical pemphigus lesions (mean

221 n frozen lesional skin of five patients with pemphigus vulgaris and five patients with pemphigus foli

222 Six of 38 pemphigus vulgaris and one of 85 normal serum samples im

223 In pemphigus vulgaris and pemphigus foliaceus (PF), autoant

224 Pemphigus vulgaris and pemphigus foliaceus are cutaneous

225 The autoantigens for pemphigus vulgaris and pemphigus foliaceus are desmoglei

226 Pemphigus vulgaris and pemphigus foliaceus are two close

227 The antigens recognized by pemphigus vulgaris and pemphigus foliaceus autoantibodie

228 rtain desmosomal blistering diseases such as pemphigus vulgaris and pemphigus foliaceus have non-cell

229 1 (Dsg1) are relevant in the pathogenesis of pemphigus vulgaris and pemphigus foliaceus, including it

230 oplastic pemphigus, as well as patients with pemphigus vulgaris and pemphigus foliaceus, were studied

231 tivator is required for blister formation in pemphigus vulgaris and pemphigus foliaceus.

232 tein kinase (MAPK) in response to pathogenic pemphigus vulgaris and PF IgG.

233 in monoclonal antibodies from a patient with pemphigus vulgaris and show that such antibodies have re

234 desmocollin 3 is a pathogenic autoantigen in pemphigus vulgaris and suggest that pemphigus vulgaris i

235 odes with accuracy >97% but only one marker, pemphigus vulgaris antigen (PVA), discriminated with 100

236 iated by autoantibodies to desmoglein 3, the pemphigus vulgaris antigen (PVA).

237 Desmoglein 3 (Dsg3), the pemphigus vulgaris antigen, has recently been shown to b

238 oliaceus and anti-desmoglein 3 antibodies in pemphigus vulgaris are pathogenic as determined by immun

239 est that the anti-desmoglein 1 antibodies in pemphigus vulgaris are pathogenic.

240 lso be at risk to develop an endemic form of pemphigus vulgaris as reported by our co-investigators f

241 of Dsg3 was thus not only restricted by the pemphigus vulgaris associated DRbeta1*0402 allele, but a

242 Of the DIF-positive cases, only pemphigus vulgaris could be diagnosed reliably by conven

243 in 1 and anti-desmoglein 3 autoantibodies in pemphigus vulgaris had predominant IgG4 subclass specifi

244 It has been postulated that the binding of pemphigus vulgaris IgG (PVIgG) to KCs induces "desmosoma

245 r formation, because pemphigus foliaceus and pemphigus vulgaris immunoglobulin G caused blisters to t

246 Pemphigus foliaceus and pemphigus vulgaris immunoglobulin G caused gross blister

247 passive transfer of pemphigus foliaceus and pemphigus vulgaris immunoglobulin G these mice blistered

248 The anti-desmoglein 1 autoantibodies in pemphigus vulgaris induced typical pemphigus foliaceus l

249 We studied patients with refractory pemphigus vulgaris involving 30% or more of their body-s

250 Pemphigus vulgaris is a blistering disease associated wi

251 tigen in pemphigus vulgaris and suggest that pemphigus vulgaris is a histological reaction pattern th

252 Pemphigus vulgaris is a life threatening bullous autoimm

253 Pemphigus vulgaris is a potentially fatal autoimmune muc

254 Pemphigus vulgaris is a rare, life-threatening autoimmun

255 ain component of the first-line treatment of pemphigus vulgaris is high doses of systemic corticoster

256 testing for IgE levels, and 30 controls with pemphigus vulgaris or pemphigus foliaceus were included

257 rative responses of T lymphocytes from eight pemphigus vulgaris patients after incubation with Dsg3 a

258 Pemphigus vulgaris patients exhibit T cell responses aga

259 ntibody blockade of desmoglein 3 function in pemphigus vulgaris patients leads to skin blistering (ac

260 first evidence that T cells from a subset of pemphigus vulgaris patients respond to both Dsg1 and Dsg

261 T cells from pemphigus vulgaris patients with no anti-Dsg1 serum reac

262 might be a target of autoantibodies in some pemphigus vulgaris patients.

263 y of the anti-desmoglein 1 autoantibodies in pemphigus vulgaris remains unknown.

264 otericin B, 3 mg/kg/d, and a young girl with pemphigus vulgaris responded to treatment with voriconaz

265 More than 50% of pemphigus vulgaris sera also contain anti-desmoglein 1 a

266 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera and examined the pathogenicity o

267 It has been well documented that a subset of pemphigus vulgaris sera have IgG reactivity to both Dsg1

268 prevented the detrimental effects induced by pemphigus vulgaris sera.

269 In pemphigus vulgaris the major pathogenic antibody binds d

270 goid; 2 cases each of linear IgA disease and pemphigus vulgaris were diagnosed; there was 1 case of b

271 tions of lesional skin from 10 patients with pemphigus vulgaris were negative for HHV8 by in situ hyb

272 Participants included 92 patients (pemphigus vulgaris, 84 [91%], and pemphigus foliaceus, 8

273 In pemphigus vulgaris, a life-threatening autoimmune skin d

274 erapeutic strategy known to be effective for pemphigus vulgaris, an autoimmune condition mediated by

275 lpha5 integrins; and sera from patients with pemphigus vulgaris, bullous pemphigoid (BP), and chronic

276 With the exception of pemphigus vulgaris, DIF is essential for establishing a

277 rate that desmocollin 3 is an autoantigen in pemphigus vulgaris, illustrated in a patient with mucosa

278 that of patients with the autoimmune disease pemphigus vulgaris, in that the mice develop spontaneous

279 rated positive DIF findings and consisted of pemphigus vulgaris, mucous membrane pemphigoid, lichen p

280 imilar to those that are highly prevalent in pemphigus vulgaris, namely DRbeta1*0402 and DRbeta1*1401

281 istologically identical to those observed in pemphigus vulgaris, suggesting that desmocollin 3 might

282 mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominant blistering in

283 ereas the anti-desmoglein 3 fraction induced pemphigus vulgaris-like lesions.

284 phigus foliaceus and fogo selvagem induced a pemphigus vulgaris-like skin disease in mice by passive

285 tis, melanoma, hidradenitis suppurativa, and pemphigus vulgaris.

286 ter solid organ transplantation and to treat pemphigus vulgaris.

287 lin is effective in patients with refractory pemphigus vulgaris.

288 vs) from a patient with active mucocutaneous pemphigus vulgaris.

289 We also show that DSG4 is an autoantigen in pemphigus vulgaris.

290 stleman's disease) nor from 19 patients with pemphigus vulgaris.

291 ic options are warranted in the treatment of pemphigus vulgaris.

292 disease course distinct from pathogenesis of pemphigus vulgaris.

293 lticenter studies for rare diseases, such as pemphigus vulgaris.

294 ents with other blistering disorders such as pemphigus vulgaris.

295 Patients had a confirmed diagnosis of pemphigus vulgaris/foliaceus, bullous pemphigoid, epider

296 tients with a primary inpatient diagnosis of pemphigus was $74466305, with a mean (SD) annual cost of

297 formation and keratinocyte susceptibility in pemphigus were discussed.

298 0.19] years for those without a diagnosis of pemphigus) were studied.

299 al blistering also occur in individuals with pemphigus (which is due to autoantibodies directed again

300 Pemphigus, which if left untreated is almost always fata