ライフサイエンスコーパス: Dsg3

1 target the desmosomal cadherin desmoglein-3 (Dsg3).

2 ated by autoantibodies against desmoglein-3 (Dsg3).

3 keratinocyte adhesion protein desmoglein 3 (Dsg3).

4 toantibodies (autoAbs) against desmoglein 3 (Dsg3).

5 ibody binding to desmoglein 1 and/or 3 (dsg1/dsg3).

6 gainst the desmosomal cadherin desmoglein-3 (Dsg3).

7 ely originates from a non-junctional pool of Dsg3.

8 eted followed by loss of detergent-insoluble Dsg3.

9 kb of 18q12 and is situated between DSG1 and DSG3.

10 ree antigenic fragments on the ectodomain of Dsg3.

11 ce that carry a spontaneous null mutation in Dsg3.

12 or tertiary (3 degrees) T cell responses to Dsg3.

13 a1*1401, also mount T cell responses against Dsg3.

14 upon 2 degrees or 3 degrees stimulation with Dsg3.

15 s vulgaris patients respond to both Dsg1 and Dsg3.

16 ies interfering with an adhesion function of Dsg3.

17 whereas the remaining four reacted only with Dsg3.

18 his study has minimal sequence homology with Dsg3.

19 keratin 14 and the desmoglein genes DSG1 and DSG3.

20 have defined this molecule as a desmoglein, DSG3.

21 g, cultured keratinocytes through binding to Dsg3.

22 d in the response to an antigen unrelated to DSG3.

23 Here, we found that Dsg3(AA145-192)-specific cells preferentially utilize th

24 t appears that Valpha22 gene is expressed by Dsg3(AA145-192)-specific cells, whereas the Valpha10 gen

25 rentially utilize the TCRVbeta13 gene, while Dsg3(AA240-303)- and Dsg3 (AA570-614)-specific cells uti

26 e Valpha10 gene is predominantly utilized by Dsg3(AA240-303)-specific T cells.

27 TCRVbeta13 gene, while Dsg3(AA240-303)- and Dsg3 (AA570-614)-specific cells utilize Vbeta7 and Vbeta

28 ha gene in the group of cells proliferate to Dsg3 (AA570-614).

29 p38 MAPK activation and its association with DSG3, abrogated p38 MAPK-induced keratin filament retrac

30 observations suggest that PV IgG binding to dsg3 activates desmosomal signal transduction cascades l

31 roteins, and demonstrate that either Dsg1 or Dsg3 alone is sufficient to maintain keratinocyte adhesi

32 duced from a PV patient causes a decrease of Dsg3 and desmoplakin but not desmocollin (Dsc) 3 in the

33 Dsg3 and Dsg1 are members of the desmoglein subfamily of

34 igus vulgaris patients after incubation with Dsg3 and Dsg1 fusion proteins.

35 dies to the desmoglein (DSG) family proteins DSG3 and DSG1, leading to loss of keratinocyte cell adhe

36 ing PV is characterized by autoantibodies to Dsg3 and Dsg1.

37 rated binding to Dsg3 or Dsg1 alone, or both Dsg3 and Dsg1.

38 (Dsg) 1; PV autoantibodies bind Dsg3 or both Dsg3 and Dsg1.

39 These data demonstrate cross-talk between dsg3 and EGFR, that this cross-talk is regulated by p38,

40 stal structures of ectodomains from Dsg2 and Dsg3 and from Dsc1 and Dsc2 show binding through a stran

41 y enhancing both the depletion of desmosomal DSG3 and intercellular adhesion defects.

42 Subsequently, Dsg3 and other desmosomal components rearrange into line

43 PKP-1 prevents loss of Dsg3 and other desmosomal proteins from cell-cell border

44 tant for keratinocyte cohesion compared with Dsg3 and that the latter forms a complex with p38 MAPK.

45 eproduce the effects of polyclonal PV IgG on Dsg3 and will facilitate future studies to further disse

46 target the desmosomal cadherin desmoglein 3 (Dsg3) and compromise keratinocyte cell-cell adhesion.

47 s foliaceus autoantibodies are desmoglein-3 (Dsg3) and desmoglein-1 (Dsg1), respectively.

48 targeting desmosomal cadherins desmoglein 3 (DSG3) and DSG1, leading to loss of keratinocyte cohesion

49 o desmosomal adhesion proteins desmoglein 3 (Dsg3) and Dsg1.

50 utoantibodies directed against desmoglein 3 (Dsg3) and/or desmoglein 1(Dsg1).

51 etween disease activity, the ELISA index for Dsg3, and/or IIF findings can occur in PV.

52 Here, we clone anti-Dsg3 antibodies (Abs) from four PV patients and identify

53 IF result was negative.OBSERVATIONS The anti-Dsg3 antibodies of our patient mainly recognized Ca2+-de

54 Anti-Dsg3 antibodies were detected in 53 of 146 normal subjec

55 and mucous membrane that coexpress Dsg1 and Dsg3, antibodies against either desmoglein alone do not

56 ent with PV in remission,who had a high anti-Dsg3 antibody ELISA index while the IIF result was negat

57 whereas the signaling of anti-desmoglein 3 (Dsg3) antibody involved JNK and biphasic p38 MAPK activa

58 dings identify the cis-adhesive interface of DSG3 as the immunodominant region targeted by pathogenic

59 of cell adhesion by altering the dynamics of Dsg3 assembly into desmosomes and the turnover of cell s

60 hosphorylation that could be responsible for Dsg3-associated cancer metastasis.

61 To define the mechanisms by which Dsg3 autoantibodies disrupt keratinocyte adhesion, the f

62 e sought to determine the prevalence of anti-Dsg3 autoantibodies in sera from normal subjects living

63 Pathogenic PV dsg3 autoantibodies were used to initiate desmosome sign

64 s of skin and mucosae and anti-desmoglein-3 (Dsg3) autoantibodies bound to the surface of lesional ke

65 se patients that exhibited the combined Dsg1/Dsg3 autoantibody reactivity showed a proliferative resp

66 6 Abs require few to no mutations to acquire Dsg3 autoreactivity, which may favour their early select

67 anti-Dsg3 response, as well as whether anti-Dsg3 B cells are Ag selected.

68 ximab that induced long-term remission, anti-Dsg3 B-cell clones were undetectable.

69 of the Dsg3 gene and the "balding" Dsg3(bal)/Dsg3(bal) mice that carry a spontaneous null mutation in

70 mutation of the Dsg3 gene and the "balding" Dsg3(bal)/Dsg3(bal) mice that carry a spontaneous null m

71 c cytotoxicity against cells expressing anti-Dsg3 BCRs in vitro and expand, persist, and specifically

72 PK links autoantibody-mediated inhibition of DSG3 binding to skin blistering.

73 f five VH1-46 germline-reverted Abs maintain Dsg3 binding, compared with zero of five non-VH1-46 germ

74 combination are necessary and sufficient for Dsg3 binding.

75 y expressing exogenous Dsg3, thereby driving Dsg3 biosynthesis and desmosome assembly.

76 PV mAbs that cause endocytosis of Dsg3 but do not dissociate keratinocytes because of comp

77 c mAbs cause internalization of cell-surface Dsg3 but not Dsc3 through early endosomes.

78 g the interaction of activated p38 MAPK with Dsg3 but not with Dsg2.

79 eactivity showed a proliferative response to Dsg3, but not to Dsg1.

80 We also showed that bal mice lack Dsg3 by IF, have typical PV oral lesions, and have a DSG

81 s, p38 knockdown prevents loss of desmosomal Dsg3 by PV mAbs, and exogenous p38 activation causes int

82 Dsg3 CAAR-T cells exhibit specific cytotoxicity against

83 Therefore, DSG3 can be a useful ancillary marker to separate SQCC f

84 vations demonstrate that T cell responses to Dsg3 can be detected in PV patients and in healthy donor

85 s (PV), autoantibodies against desmoglein 3 (Dsg3) cause loss of cell-cell adhesion of keratinocytes

86 s bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell detachment (acantholy

87 lation experiments demonstrated that soluble Dsg3 cell surface pools were rapidly depleted followed b

88 Using a series of Dsg3 chimeras and deletion constructs, we find that PKP-

89 rization, we could no longer detect any anti-Dsg3 clones in PV1 by APD.

90 ever, acantholytic cells retain cell surface Dsg3 compared with wild-type mice.

91 Furthermore, the internalized PV IgG-Dsg3 complex colocalized with markers for both endosomes

92 The PV IgG.Dsg3 complex failed to colocalize with clathrin, and inh

93 Dsg3 complexes localized at the cell surface are transpo

94 Furthermore, the Dsg3 cytoplasmic tail specified sensitivity to these inh

95 n and keratin filament retraction induced by Dsg3 depletion is ameliorated by specific p38 MAPK inhib

96 Because loss of cell cohesion and Dsg3 depletion is observed in the autoantibody-mediated

97 Moreover, because loss of cell adhesion by Dsg3 depletion was partially rescued by p38 MAPK inhibit

98 by reversing Ca(2+) insensitivity, promotes Dsg3 depletion.

99 ous p38 activation causes internalization of Dsg3, desmocollin 3, and desmoplakin.

100 antibodies against the desmosomal cadherin, DSG3 (desmoglein-3), cause acantholysis.

101 the normal tissue distributions of Dsg1 and Dsg3 determine the sites of blister formation.

102 rown from Dsg3(-/-) mice, we determined that Dsg3 did not serve as a surrogate antigen allowing antim

103 These changes in Dsg3 distribution are followed by depletion of detergent

104 y cause internalization of newly synthesized Dsg3 during desmosome assembly, correlating with their p

105 eal epithelial cells did not express Dsc3 or Dsg3 during re-epithelialization.

106 h N- and COOH-terminal epitopes of the human Dsg3 ectodomain.

107 Within 6 h after PV IgG binding to Dsg3, electron microscopy revealed that desmosomes were

108 ncing of MK2 expression block PV mAb-induced Dsg3 endocytosis in human keratinocytes.

109 termine the relationship between p38MAPK and DSG3 endocytosis in pemphigus.

110 in- and dynamin-independent pathway and that Dsg3 endocytosis is tightly coupled to the pathogenic ac

111 Moreover, inhibition of Dsg3 endocytosis with genistein prevented disruption of

112 These findings demonstrate that Dsg3 endocytosis, keratin filament retraction, and the l

113 Inhibition of EGFR blocked PV IgG-triggered dsg3 endocytosis, keratin intermediate filament retracti

114 unction downstream to augment blistering via Dsg3 endocytosis.

115 between these indexes and anti-Dsg1 and anti-Dsg3 enzyme-linked immunosorbent assay values has not be

116 Serum anti-Dsg1 and anti-Dsg3 enzyme-linked immunosorbent assay values were measu

117 at CD4(+) T cells recognizing immunodominant Dsg3 epitopes in the context of the PV-associated HLA-DR

118 04:02-restricted T cell recognition of human Dsg3 epitopes leads to the induction of pathogenic IgG A

119 These findings suggest that the Dsg3 epitopes targeted by pathogenic mPV IgG are human s

120 e of this study was to determine the role of DSG3 expression in the diagnosis of SQCCs of the lung an

121 tent with this hypothesis, we found Dsg1 and Dsg3 expression overlapping in the companion layer.

122 the pathogenic antibodies were mapped to the DSG3 extracellular 1 (EC1) and EC2 subdomains, regions i

123 tor measurements in keratinocytes showed the Dsg3 extracellular domain is ordered at the individual d

124 sults demonstrate the critical importance of Dsg3 for adhesion in deep stratified squamous epithelia

125 stochemistry, sensitivity and specificity of DSG3 for lung cancers were 98% and 99%, respectively.

126 We showed that Dsg3 formed a complex with Ezrin at the plasma membrane

127 utants resulted in loss of cell cohesion and Dsg3 fragmentation.

128 , we isolated 15 IgG antibodies specific for DSG3 from 2 PV patients.

129 st, pathogenic mAbs caused late depletion of Dsg3 from preformed desmosomes at 24 hours, with effects

130 cytes with PV IgG causes a redistribution of DSG3 from the cell surface to endosomes, which target th

131 ve response after exposure to either Dsg1 or Dsg3 fusion proteins.

132 In this study, we have cloned the human DSG3 gene and examined the transcriptional regulation of

133 3(null) mice with a targeted mutation of the Dsg3 gene and the "balding" Dsg3(bal)/Dsg3(bal) mice tha

134 Targeted disruption of the Dsg3 gene by homologous recombination (Dsg3tm1stan) in m

135 ion of up-regulated expression levels of the DSG3 gene in pulmonary squamous cell carcinomas (SQCCs).

136 IF, have typical PV oral lesions, and have a DSG3 gene mutation.

137 dentified a 14 bp deletion in exon 13 of the Dsg3 gene resulting in a frameshift and premature termin

138 ygous for a 1 bp insertion (2275insT) in the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA.

139 eered mice with a targeted disruption of the DSG3 gene.

140 The microarray data showed that DSG3 had a sensitivity and specificity of 88% and 98%, r

141 Autoantibodies against desmoglein 3 (Dsg3) have also been detected in sera from patients with

142 We therefore generated a fully humanized Dsg3 (hDSG3) murine model utilizing a hDsg3 transgenic a

143 Characterization of the anti-Dsg3 IgG(+) repertoire by antibody phage display (APD) a

144 ediated disease, in which anti-desmoglein 3 (Dsg3) IgG autoantibodies cause life-threatening blisteri

145 Th2-like cytokine profile, and responding of Dsg3 in a restriction to HLA-DRBI*0402 or 1401 alleles.

146 Ectopic expression of Dsg3 in cancer cell lines caused enhanced phosphorylatio

147 evertheless, because subsequent targeting of Dsg3 in Dsg2-depleted cells led to drastically enhanced

148 the hypothesis that coexpression of Dsg1 and Dsg3 in keratinocytes protects against pathology due to

149 Expression of Dsc3 and Dsg3 in limbus and conjunctiva coincides with their asso

150 esized that Dsg1 compensates for the loss of Dsg3 in the anagen hair follicles of these Dsg3-/- mice.

151 udy, we compared the involvement of Dsg2 and Dsg3 in the p38 MAPK-dependent regulation of keratinocyt

152 mpanion layer, and particularly the Dsg1 and Dsg3 in this layer, in anchoring the anagen hair to the

153 ed desmoglein (Pemphigus Vulgaris Antigen or Dsg3) in cells known to express its wild-type counterpar

154 der of the desmosomal cadherin desmoglein 3 (Dsg3) in living cells.

155 scribed in B cells reacting to desmoglein 3 (Dsg3) in the autoimmune disease pemphigus vulgaris (PV),

156 ion of the desmosomal cadherin desmoglein 3 (DSG3) in the pathogenesis of PV.

157 ored desmosome-containing pool revealed that Dsg3, in contrast to Dsg2, is present in relevant amount

158 Over 90% are specific for both Dsg1 and Dsg3 indicating extensive cross-reactivity between these

159 pletion of Dsg2, siRNA-mediated silencing of Dsg3 induced p38 MAPK activation, which is in line with

160 cells recognizing immunodominant epitopes of Dsg3 initiate the production of Dsg3-reactive IgG autoan

161 Cell-surface DSG3 internalization and depletion from both the deterge

162 APK is capable of regulating PV IgG-mediated DSG3 internalization and that previously isolated mechan

163 r, these results suggest that PV IgG-induced Dsg3 internalization is mediated through a clathrin- and

164 Dsg3 internalization was associated with retraction of k

165 docytic machinery involved in PV IgG-induced Dsg3 internalization, human keratinocytes were incubated

166 ing KCs demonstrated that PV IgG cause rapid Dsg3 internalization, which likely originates from a non

167 ependent pathways had little or no effect on Dsg3 internalization.

168 e inhibitor genistein dramatically inhibited Dsg3 internalization.

169 V IgG causes internalization of cell-surface DSG3 into endosomes (as early as 4 h), which are then de

170 e and trigger its internalization along with DSG3 into the endosomal pathway, where it is ultimately

171 epidermis of normal mice) where Dsg1 without Dsg3 is expressed, anti-Dsg1 antibodies alone can cause

172 tudies demonstrate that upon PV IgG binding, Dsg3 is internalized and enters an endo-lysosomal pathwa

173 esides its function as an adhesion molecule, Dsg3 is strengthening cell cohesion via modulation of p3

174 tor receptor and Src was affected neither in Dsg3(-/-) KCs nor due to absorption of antimitochondrial

175 tion of interacting with F-actin and CD44 as Dsg3 knockdown impaired these associations.

176 ion and Dsg2 was enhanced at the membrane in Dsg3 knockout cells, we conclude that Dsg2 compensates f

177 cells, we conclude that Dsg2 compensates for Dsg3 loss of function.

178 eratinocytes with pathogenic monovalent anti-Dsg3 mAbs produced from a PV patient causes a decrease o

179 autoantibodies that fail to recognize murine Dsg3 (mDsg3); thus, passive transfer experiments of mPV

180 Taken together, our study identifies a novel Dsg3-mediated c-Jun/AP-1 regulatory mechanism and PKC-de

181 To test whether Dsg3 mediates adhesion, we genetically engineered mice w

182 DSG3 -/- mice had no DSG3 mRNA by RNase protection assay

183 The runting and hair loss phenotype of DSG3 -/- mice is identical to that of a previously repor

184 Using KCs grown from Dsg3(-/-) mice, we determined that Dsg3 did not serve as

185 vement in the clinical manifestations of the Dsg3(-/-) mice.

186 ion of ETA, Dsg3-/- mice, but not Dsg3+/+ or Dsg3+/- mice, showed striking loss of anagen hair, which

187 The oral lesions in DSG3-/- mice reduce their food intake, resulting in a ru

188 Four hours after injection of ETA, Dsg3-/- mice, but not Dsg3+/+ or Dsg3+/- mice, showed st

189 oliative toxin A (ETA) to inactivate Dsg1 in Dsg3-/- mice.

190 f Dsg3 in the anagen hair follicles of these Dsg3-/- mice.

191 DSG3 -/- mice had no DSG3 mRNA by RNase protection assay and no Dsg3 protein

192 We demonstrate that, although a Dsg3 mRNA transcript was detectable in Dsg3bal-Pas skin,

193 Expression of DSG3 mRNA was evaluated in bulk laser capture microdisse

194 n the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA.

195 We used both the Dsg3(null) mice with a targeted mutation of the Dsg3 gen

196 liaceus IgGs produce a distinct phenotype in Dsg3(null) mice.

197 sive transfer of pemphigus IgG to normal and DSG3(null) neonatal mice, we show that in the areas of e

198 filament retraction, and promoted desmosomal DSG3 oligomerization.

199 ated by autoantibodies against desmoglein 3 (Dsg3) on epidermal keratinocytes.

200 used by autoantibodies against desmoglein 3 (Dsg3) on epidermal keratinocytes.

201 t desmoglein (Dsg) 1; PV autoantibodies bind Dsg3 or both Dsg3 and Dsg1.

202 olecules between human Dsg1 and either human Dsg3 or canine Dsg1, we show that for cleavage, human-sp

203 ScFv mAbs demonstrated binding to Dsg3 or Dsg1 alone, or both Dsg3 and Dsg1.

204 al at birth, but by 8-10 d weighed less than DSG3 +/- or +/+ littermates, and at around day 18 were g

205 Utilizing a desmoglein-3 mouse model (Dsg3(-/-)) or keratin 5-specific reporter mice, the inve

206 fter injection of ETA, Dsg3-/- mice, but not Dsg3+/+ or Dsg3+/- mice, showed striking loss of anagen

207 Live cell imaging revealed Dsg3 order decreased more rapidly (lambda = 5.5 min), in

208 re 2 methods that are widely used to measure Dsg3 orDsg1 antibody titers in PV.

209 phosphorylation, among others, was found in Dsg3-overexpressing cells and the activation of c-Jun/AP

210 The increased Ezrin phosphorylation in Dsg3-overexpressing cells could be abrogated substantial

211 ical study using antibodies directed against DSG3, p63, and CK5/6 was also performed.

212 g3-reactive CD4(+) T cells by distinct human Dsg3 peptides that bind to HLA-DRbeta1*04:02 is tightly

213 major T cell population stimulated by these Dsg3 peptides was CD4 positive.

214 Using Dsg3 peptides, one immunodominant peptide (residues 161-

215 patients responded to at least one of three Dsg3 peptides.

216 ther patient groups did not respond to these Dsg3 peptides.

217 followed by depletion of detergent-insoluble Dsg3 pools and by the loss of cell adhesion strength.

218 series of deletion clones indicated that the DSG3 promoter demonstrated keratinocyte-specific express

219 o DSG3 mRNA by RNase protection assay and no Dsg3 protein by immunofluorescence (IF) and immunoblots.

220 s from two normals were also stimulated by a Dsg3 protein devoid of the EC2-3 (deltaN1), suggesting t

221 conformational epitopes and targeted mature Dsg3 protein.We report this case focusing on the discrep

222 RNAs that silenced expression of Dsg1 and/or Dsg3 proteins, blocked approximately 50% of p38 MAPK act

223 Finally, these results identify Dsg3-reactive CD4(+) T cells as potential therapeutic ta

224 Activation of Dsg3-reactive CD4(+) T cells by distinct human Dsg3 pept

225 epitopes of Dsg3 initiate the production of Dsg3-reactive IgG autoantibodies is still missing.

226 ino acid residues predisposing VH1-46 Abs to Dsg3 reactivity reside in CDR2.

227 eactivity; most mutations abolish VP6 and/or Dsg3 reactivity.

228 Here, we report that Dsg3 regulates the activity of c-Jun/AP-1 as well as pro

229 autoantibodies against desmoglein (Dsg)1 and Dsg3, respectively.

230 tigen BP180 and desmosomal antigens Dsg1 and Dsg3, respectively.

231 sing the diversity and clonality of the anti-Dsg3 response, as well as whether anti-Dsg3 B cells are

232 The Dsg3 responses of these T cells were restricted to HLA-D

233 ted against the desmosomal adhesion molecule Dsg3, resulting in severe mucosal erosions and epidermal

234 tibility complex class II alleles restricted Dsg3 specific T cell responses.

235 expand, persist, and specifically eliminate Dsg3-specific B cells in vivo.

236 iated HLA-DRB1*04:02 induce the secretion of Dsg3-specific IgG in vivo.

237 Two CD4+ Dsg3-specific T cell lines and 12 T cell clones from two

238 Dsg3-specific T cell lines and clones were developed and

239 toantibodies is presumably T cell dependent, Dsg3-specific T cell reactivity was investigated in 14 P

240 T cell epitope(s) and TCR genes utilized by Dsg3-specific T cells.

241 immunoreactive segments of the ectodomain of Dsg3 specifically induced proliferation of T cells from

242 is sera have IgG reactivity to both Dsg1 and Dsg3, suggesting that Dsg1 may also participate in the a

243 ent on the plakoglobin-binding domain of the Dsg3 tail.

244 is patients exhibit T cell responses against Dsg3 that may serve as a target to modulate the producti

245 gainst the desmosomal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause loss of epider

246 Desmoglein 3 (Dsg3), the pemphigus vulgaris antigen, has recently been

247 bly can be prevented by expressing exogenous Dsg3, thereby driving Dsg3 biosynthesis and desmosome as

248 es and the turnover of cell surface pools of Dsg3 through endocytic pathways.

249 autoantibody-mediated direct interference of DSG3 transinteraction, as revealed by atomic force micro

250 By limiting loss of DSG3 transinteraction, p38 MAPK activation, and keratin

251 -46 B cell populations may be predisposed to Dsg3-VP6 cross-reactivity, but multiple mechanisms preve

252 whether VH1-46 B cells may be predisposed to Dsg3-VP6 cross-reactivity.

253 wever, somatic mutations only rarely promote Dsg3-VP6 cross-reactivity; most mutations abolish VP6 an

254 Depletion of Dsg3 was inhibited by DP-S2849G-GFP in the cytoskeletal

255 Remarkably, binding to DSG3 was lost when somatic mutations were reverted to th

256 DSG3 was over-expressed in SQCCs but had very limited ex

257 oth endosomes and lysosomes, suggesting that Dsg3 was targeted for degradation.

258 T cell recognition of Dsg3 was thus not only restricted by the pemphigus vulga

259 T cell responses to Dsg3 were also observed in four of 12 healthy individual

260 sg2) were expressed throughout, but Dsc3 and Dsg3 were confined to the limbus and conjunctiva, and Ds

261 orescence analysis indicated that PV IgG and Dsg3 were rapidly internalized from the cell surface in

262 stronger in superficial layers, but Dsc3 and Dsg3 were stronger basally, fading suprabasally.

263 Antibodies against BP180, Dsg1, and Dsg3, when injected into neonatal mice, induce the BP, P

264 atients showed reactivity with both Dsg1 and Dsg3, whereas the remaining four reacted only with Dsg3.

265 taining the extracellular portion (EC1-5) of Dsg3, whereas two of seven PV patients in remission or u

266 Comparison of exon-intron organization of DSG3 with bovine DSG1 and several classical cadherin gen

267 DRbeta1*0402+ patient PV9 was stimulated by Dsg3 with DRbeta1*0402+ L cells as antigen-presenting ce

268 donor C11 were differentially stimulated by Dsg3 with L cells expressing one of several DR11 alleles

269 iagnosis of SQCCs of the lung and to compare DSG3 with p63, CK5, and CK6, as markers of squamous cell

270 tion constructs, we find that PKP-1 clusters Dsg3 with the desmosomal plaque protein desmoplakin in a