ライフサイエンスコーパス: pemphigus

1 s an effective and safe treatment option for pemphigus.

2 icacious and well tolerated in patients with pemphigus.

3 tibodies in skin blistering diseases such as pemphigus.

4 t EGFR is a potential therapeutic target for pemphigus.

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

6 investigating the use of EGFR inhibitors in pemphigus.

7 ation in the passive transfer mouse model of pemphigus.

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

9 f T cells responsible for the development of pemphigus.

10 fluorescence were negative, excluding an IgA pemphigus.

11 ship between p38MAPK and DSG3 endocytosis in pemphigus.

12 mechanisms for the loss of cell adhesion in pemphigus.

13 sts are effective for treating patients with pemphigus.

14 bility of specific autoantibody targeting in pemphigus.

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

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

17 utoimmune blistering disease, paraneoplastic pemphigus.

18 acantholysis in the neonatal mouse model of pemphigus.

19 ments possibly underlying the paraneoplastic pemphigus.

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

21 tiation of the autoimmune blistering disease pemphigus.

22 ittle is known about the inpatient burden of pemphigus.

23 were all associated with hospitalization for pemphigus.

24 tions by Trichosporon inkin in patients with pemphigus.

25 oor outcome in patients with severe forms of pemphigus.

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

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 proposed to provide an objective measure of pemphigus activity.

30 scores are robust tools to accurately assess pemphigus activity.

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

32 Pemphigus and bullous pemphigoid are autoantibody-mediat

33 Pemphigus and bullous pemphigoid are distinct autoimmune

34 e major autoimmune blistering skin diseases, pemphigus and bullous pemphigoid.

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

36 e critically involved in the pathogenesis of pemphigus and offer novel targets for therapeutic interv

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

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

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

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

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

42 -dominated immune signature in patients with pemphigus, and Kyoto Encyclopedia of Genes and Genomes p

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

44 contributions to potential pathogenicity of pemphigus antibodies, bead assays coated with recombinan

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

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

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

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

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

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

51 mosomal cadherins, including human and mouse pemphigus autoantibodies, had no effect on monolayer int

52 determine the epitopes and pathogenicity of pemphigus autoantibodies.

53 ameliorated loss of cell adhesion induced by pemphigus autoantibodies.

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

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

56 a valuable adjunctive therapy for control of pemphigus blistering.

57 ng systemic lupus erythematosus, angioedema, pemphigus, bullous pemphigoid, and HS.

58 Pemphigus bursarius is a host-alternating aphid in which

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

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

61 Pemphigus consists of a group of rare and severe autoimm

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

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

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

65 The Pemphigus Disease Area Index (PDAI) and Autoimmune Bullo

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

67 0.69; P = .009) and low correlation with the Pemphigus Disease Area Index (R = 0.42) and Autoimmune B

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

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

70 Pemphigus encompasses a group of autoimmune blistering d

71 ly maxadilan and LJM11, have been related to pemphigus etiopathogenesis in the New World, being propo

72 The pemphigus family of autoimmune bullous disorders is char

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

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

75 patients with pemphigus vulgaris (n = 84) or pemphigus foliaceus (n = 32) were included.

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

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

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

79 Pemphigus foliaceus (PF) is a blistering disease caused

80 Pemphigus foliaceus (PF) is a human autoimmune blisterin

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

82 Pemphigus foliaceus (PF) is an autoimmune skin blisterin

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

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

85 but also overlaps with an endemic focus for pemphigus foliaceus (PF), also known as Fogo Selvagem.

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

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

88 In pemphigus foliaceus (PF), autoantibodies against desmogl

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

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

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

92 All sera tested from eight patients with pemphigus foliaceus and eight patients with mucosal pemp

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

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

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

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

97 glein (Dsg) 1 and Dsg3 IgG autoantibodies in pemphigus foliaceus and pemphigus vulgaris cause blister

98 After passive transfer of pemphigus foliaceus and pemphigus vulgaris immunoglobuli

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

100 Pemphigus foliaceus and pemphigus vulgaris immunoglobuli

101 c is important for disease pathology in both pemphigus foliaceus and pemphigus vulgaris.

102 aired sera obtained from seven patients with pemphigus foliaceus and six patients with pemphigus vulg

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

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

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

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

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

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

109 Pemphigus foliaceus is an autoimmune blistering skin dis

110 Pemphigus foliaceus is an autoimmune skin disease mediat

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

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

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

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

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

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

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

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

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

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

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

122 n originates with painful oral erosions, and pemphigus foliaceus, which is characterised by exclusive

123 patients with pemphigus vulgaris and 2 with pemphigus foliaceus.

124 blister formation in pemphigus vulgaris and pemphigus foliaceus.

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

126 w cytometry showed that patients with active pemphigus had elevated levels of circulating IL-17(+)(,)

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

128 r PDAI were higher in moderate and extensive pemphigus (ICC = 0.82, 95% CI = 0.63-0.92 and ICC = 0.80

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

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

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

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

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

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

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

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

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

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

139 Pemphigus is a life-threatening autoimmune disease in wh

140 Pemphigus is a life-threatening blistering disorder of t

141 Pemphigus is a rare autoimmune disease that results in b

142 Pemphigus is an autoimmune blistering disorder associate

143 Pemphigus is an autoimmune disease of skin adhesion asso

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

145 Pemphigus is diagnosed on the basis of either IgG or com

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

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

148 In pemphigus, keratinocytes in epidermis and mucous membran

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

150 to determine differential gene expression in pemphigus lesions and skin of healthy individuals.

151 Pemphigus lesions are mediated directly by the autoantib

152 levated tissue-type plasminogen activator in pemphigus lesions.

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

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

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

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

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

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

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

160 However, the role of other T-cell subsets in pemphigus pathogenesis remained unclear.

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

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

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

164 the relevance of the apoptotic mechanism in pemphigus pathogenesis.

165 are blocked by autoantibodies from multiple pemphigus patients.

166 histologically similar to those observed in pemphigus patients.

167 n and mucocutaneous acantholysis observed in pemphigus patients.

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

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

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

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

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

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

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

175 7(+) memory B cells, and patients with acute pemphigus showed higher levels of Dsg3-autoreactive T(FH

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

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

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

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

180 The two main pemphigus variants are pemphigus vulgaris, which often o

181 A total of 116 patients with pemphigus vulgaris (n = 84) or pemphigus foliaceus (n =

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

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

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

185 receptor T cells (DSG3-CAART) expressing the pemphigus vulgaris (PV) autoantigen DSG3 fused to CD137-

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

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

188 Pemphigus vulgaris (PV) encompasses two clinical phenoty

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

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

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

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

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

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

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

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

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

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

199 Pemphigus vulgaris (PV) is a potentially fatal autoimmun

200 Pemphigus vulgaris (PV) is a potentially fatal autoimmun

201 Pemphigus vulgaris (PV) is a potentially fatal blisterin

202 Pemphigus vulgaris (PV) is a potentially fatal blisterin

203 Pemphigus vulgaris (PV) is a potentially fatal blisterin

204 Pemphigus vulgaris (PV) is a potentially lethal mucocuta

205 Pemphigus vulgaris (PV) is a potentially lethal mucocuta

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

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

208 Pemphigus vulgaris (PV) is an autoimmune blistering dise

209 Pemphigus vulgaris (PV) is an autoimmune blistering dise

210 Pemphigus vulgaris (PV) is an autoimmune blistering dise

211 Pemphigus vulgaris (PV) is an autoimmune bullous disease

212 Pemphigus vulgaris (PV) is an autoimmune disease mediate

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

214 Pemphigus vulgaris (PV) is an autoimmune epidermal blist

215 Pemphigus vulgaris (PV) is an epidermal blistering disor

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

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

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

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

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

221 0 antibody rituximab is highly effective for pemphigus vulgaris (PV) treatment.

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

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

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

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

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

227 Patients with the blistering skin disease pemphigus vulgaris (PV), which is caused by autoantibodi

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

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

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

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

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

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

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

235 Pemphigus vulgaris and pemphigus foliaceus are two close

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

237 1 (Dsg1) are relevant in the pathogenesis of pemphigus vulgaris and pemphigus foliaceus, including it

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

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

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

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

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

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

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

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

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

247 gG autoantibodies in pemphigus foliaceus and pemphigus vulgaris cause blisters through loss of desmos

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

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

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

251 Pemphigus foliaceus and pemphigus vulgaris immunoglobulin G caused gross blister

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

253 th pemphigus foliaceus and six patients with pemphigus vulgaris in active disease and remission were

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

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

256 Pemphigus vulgaris is a blistering disease associated wi

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

258 Pemphigus vulgaris is a potentially fatal autoimmune muc

259 Pemphigus vulgaris is a rare, life-threatening autoimmun

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

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

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

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

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

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

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

267 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera and examined the pathogenicity o

268 prevented the detrimental effects induced by pemphigus vulgaris sera.

269 In pemphigus vulgaris the major pathogenic antibody binds d

270 us foliaceus and eight patients with mucosal pemphigus vulgaris with active disease inhibited the adh

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

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

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

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

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

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

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

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

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

280 The two main pemphigus variants are pemphigus vulgaris, which often originates with painful

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

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

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

284 ents with other blistering disorders such as pemphigus vulgaris.

285 ter solid organ transplantation and to treat pemphigus vulgaris.

286 se pathology in both pemphigus foliaceus and 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 tis, melanoma, hidradenitis suppurativa, and 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 Patients had a confirmed diagnosis of pemphigus vulgaris/foliaceus, bullous pemphigoid, epider

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

296 formation and keratinocyte susceptibility in pemphigus were discussed.

297 Consecutive patients with newly diagnosed pemphigus were enrolled in 31 centers.

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