ライフサイエンスコーパス: vitiligo

1 this form can be associated with NSV (mixed vitiligo).

2 e-high niche in both a mouse model and human vitiligo.

3 ibitors may be effective in the treatment of vitiligo.

4 imvastatin may be an effective treatment for vitiligo.

5 and interfollicular epidermis of UV-treated vitiligo.

6 or the melanocyte biology and development of vitiligo.

7 ance of depigmentation in our mouse model of vitiligo.

8 pidermis, which was lacking in the untreated vitiligo.

9 targeted treatment option for patients with vitiligo.

10 y to support repigmentation in patients with vitiligo.

11 B) phototherapy is used extensively to treat vitiligo.

12 biomarkers and therapeutic targets in human vitiligo.

13 continental variation for rates of extensive vitiligo.

14 lly early in life, play an important role in vitiligo.

15 ation and mitochondrial energy metabolism in vitiligo.

16 oma-initiated, self-perpetuating, autoimmune vitiligo.

17 ddressed the mechanism regulating autoimmune vitiligo.

18 se progressive depigmentation and autoimmune vitiligo.

19 ulate in the skin of MT/ret mice with active vitiligo.

20 ng lymph nodes of MT/ret mice not developing vitiligo.

21 ovel and potentially effective treatment for vitiligo.

22 s melanoma, autoimmune disease, or cutaneous vitiligo.

23 nnate immune activation promote the onset of vitiligo.

24 fying 14 susceptibility loci for generalized vitiligo.

25 antly lower TPH1 expression in patients with vitiligo.

26 cient TRP1-specific CD4(+) T cells to induce vitiligo.

27 idermal redox balance and immune response in vitiligo.

28 zyl ether of hydroquinone, known triggers of vitiligo.

29 e following exposure to chemical triggers of vitiligo.

30 and activation as well as treatment-related vitiligo.

31 excellent animal model for human autoimmune vitiligo.

32 attempted to comprehend the genetic basis of vitiligo.

33 llicular melanocytes, the primary targets in vitiligo.

34 inflammatory myositis, Raynaud's disease and vitiligo.

35 matological conditions such as psoriasis and vitiligo.

36 0B as a potential disease activity marker in vitiligo.

37 by the tumor, and did not induce autoimmune vitiligo.

38 actions to sun exposure and risk of incident vitiligo.

39 rly (</=2 months) and advanced (>/=6 months) vitiligo.

40 , which supports their role as biomarkers in vitiligo.

41 e included and screened for the emergence of vitiligo.

42 ditional subgroup of patients with extensive vitiligo.

43 oral prednisolone with improved outcomes for vitiligo.

44 nonsegmental vitiligo and 10 with segmental vitiligo.

45 s of sCD27 and sCD25 in patients with active vitiligo.

46 alone and UV-B alone with repigmentation for vitiligo.

47 icacy and fewest adverse events for treating vitiligo?

48 t was associated with a higher occurrence of vitiligo (12 of 17 [71%] vs 14 of 50 [28%]; P = .002).

49 Fifteen (5.3%) of 282 patients demonstrated vitiligo (14 of 282; 4.9%) and/or AA (2 of 282; 0.7%) (1

50 Of the 17 patients with vitiligo, 3 (18%) had a complete response, 9 (53%) had a

51 Vitiligo, a clinically visible immune-related adverse ev

52 A total of 35% of MT/ret mice develop a vitiligo, a skin depigmentation attributable to the lysi

53 CD8+ T cells in mice with vitiligo acquired phenotypic and functional characterist

54 correlations between the S100B dynamics and vitiligo activity, identifying high circulating S100B le

55 al autoimmune diseases including generalized vitiligo, Addison disease, type 1 diabetes, rheumatoid a

56 outside the United States had lower odds of vitiligo-affected BSA greater than 25%, even after contr

57 we report a genome-wide association study of vitiligo age of onset in 1,339 generalized vitiligo pati

58 We identified a quantitative trait locus for vitiligo age of onset in the major histocompatibility co

59 In contrast, there was no association of vitiligo age of onset with any other MHC or non-MHC loci

60 s involved in vitiligo susceptibility versus vitiligo age of onset, and illustrate that genome-wide a

61 type 1, rheumatic disease, thyroid disease, vitiligo, alopecia areata and inflammatory bowel disease

62 Age of onset of generalized vitiligo also involves a substantial genetic component,

63 Vitiligo, an acquired pigmentary disorder of unknown ori

64 Vitiligo, an autoimmune disease in which skin melanocyte

65 , AIRE-deficient patients are predisposed to vitiligo, an autoimmune disease of melanocytes that is o

66 Vitiligo, an autoimmune disease of the skin, has been th

67 diseases, the questions that remain, and how vitiligo, an underappreciated example of organ-specific

68 447 participants were included in the AA and vitiligo analyses, respectively.

69 , including 83 individuals with nonsegmental vitiligo and 10 with segmental vitiligo.

70 In total, 16 studies of vitiligo and 17 studies of AA were included in the revie

71 ising 183 CEU simplex trios with generalized vitiligo and 332 CEU multiplex families.

72 yses were used to determine risk factors for vitiligo and AA development.

73 s associated with increased risk of incident vitiligo and AA in adulthood.

74 d/or AA (2 of 282; 0.7%) (1 patient had both vitiligo and AA).

75 However, vitiligo and alopecia areata (AA) have not been well cha

76 ermatitis (AD) is increased in patients with vitiligo and alopecia areata (AA).

77 were performed for childhood vs adult-onset vitiligo and alopecia totalis or alopecia universalis vs

78 x regulation of self-reactive CD8 T cells in vitiligo and demonstrates the overall poorly immunogenic

79 t populations with generalized and localized vitiligo and in several vitiligo populations studied pre

80 biomarkers to determine disease activity in vitiligo and indicate likely future progression.

81 the mechanisms underlying melanocyte loss in vitiligo and pathways linking environmental stressors an

82 acquisition, and T-cell activation in early vitiligo and reinforce the role of melanocyte-derived CX

83 rature on the relationship between cutaneous vitiligo and uveal melanoma.

84 h uveal melanoma who had developed cutaneous vitiligo and were examined at a tertiary eye care instit

85 nded to a question about clinician-diagnosed vitiligo and year of diagnosis (2001 or before, 2002-200

86 Patients with vitiligo and/or AA were identified from dermatologist do

87 ificantly associated with the development of vitiligo and/or AA.

88 vant to both autoimmune skin depigmentation (vitiligo) and tumor immunity, because they are expressed

89 Self-reported and/or physician-diagnosed AD, vitiligo, and AA.

90 have been implicated in the pathogenesis of vitiligo, and expression of IFN-gamma is increased in th

91 We sought to identify new treatments for vitiligo, and first considered repurposed medications be

92 n and progression and in melanocyte death in vitiligo, and how this knowledge can be harnessed for me

93 eversed depigmentation in our mouse model of vitiligo, and reduced the number of infiltrating autorea

94 uman skin measurements on melanocytic nevus, vitiligo, and venous occlusion conditions were performed

95 ellular contributions during autoimmunity in vitiligo, and we found that the epidermis is a chemokine

96 A meta-analysis of studies assessing AD, vitiligo, and/or AA was performed using a fixed-effects

97 Therapeutic options for vitiligo are limited, reflecting in part limited knowled

98 responses are perpetuated in the context of vitiligo are not well understood.

99 Response on the Vitiligo Area Scoring Index and Vitiligo European Task F

100 ination therapy group had improvement in the Vitiligo Area Scoring Index at days 56 and 84 (P < .05);

101 "palm of hand 1% rule" as integrated in the Vitiligo Area Scoring Index.

102 e VES (intraclass correlation VES: 0.923 vs. Vitiligo Area Scoring Index: 0.757) was also found in an

103 e VES (intraclass correlation VES: 0.924 vs. Vitiligo Area Scoring Index: 0.846).

104 ios to determine the risk of incident AA and vitiligo associated with AD diagnosed in or before 2009.

105 termine the risk of alopecia areata (AA) and vitiligo associated with atopic dermatitis (AD) in a lar

106 ios and 95% confidence intervals of incident vitiligo associated with exposures variables, adjusting

107 nd 6,723 controls) identifying 13 additional vitiligo-associated loci.

108 Vitiligo-associated memory CD8+ T cells provided durable

109 that reported on autoimmune toxicity and/or vitiligo between 1995 and 2013.

110 the melanocytes captured from NBUVB-treated vitiligo bulge compared with untreated vitiligo bulge.

111 eated vitiligo bulge compared with untreated vitiligo bulge.

112 We developed and validated a specific vitiligo burden tool according to skin phototype.

113 We developed and validated a specific vitiligo burden tool according to skin phototype.

114 QOL instruments exist, there is no specific vitiligo burden tool.

115 life instruments exist, there is no specific vitiligo burden tool.

116 ort here a second GWAS (450 individuals with vitiligo (cases) and 3,182 controls), an independent rep

117 Variants of the Bach2 gene are linked to vitiligo, celiac disease, and type 1 diabetes, but the u

118 lanoma cells, was severely down-regulated in vitiligo cell line PIG3V and skin biopsy samples from vi

119 In this study we characterized the human vitiligo cell line PIG3V and the normal human melanocyte

120 active oxygen species production observed in vitiligo cells appear to be partly due to abnormal regul

121 and respiratory responses were defective in vitiligo cells.

122 critical regulator of cellular metabolism in vitiligo cells.

123 l patients without AA (n = 3), patients with vitiligo (Cochran-Mantel-Haenszel OR, 7.82; 95% CI, 3.06

124 Existing mouse models of vitiligo consist of hair depigmentation but lack promine

125 iscuss important clinical characteristics of vitiligo, current therapies and their limitations, advan

126 ision of costimulation results in autoimmune vitiligo, demonstrating that LECs are significant, albei

127 The vitiligo developed bilaterally with multiple well-define

128 Vitiligo developed in approximately 60% of mice that wer

129 ur results identify unexpected complexity in vitiligo development and point toward possible therapeut

130 auses, but the exact molecular mechanisms of vitiligo development and progression, particularly those

131 e depigmentation and the prognostic value of vitiligo development on survival.

132 7 studies reporting individual patient data, vitiligo development was significantly associated with b

133 respectively, compared with patients without vitiligo development.

134 , confirming a central role for IFN-gamma in vitiligo development.

135 ts included in the study, 17 (25%) developed vitiligo during pembrolizumab treatment and 50 (75%) did

136 Patients with either vitiligo, especially early-onset disease, or AA, especia

137 ponse on the Vitiligo Area Scoring Index and Vitiligo European Task Force scoring system.

138 tates) with a history of physician-diagnosed vitiligo.EXPOSURES Regions of birth and residence.

139 udy demonstrates that for risk of autoimmune vitiligo, expression level of HLA class II molecules is

140 proposed as a promising tool to measure the vitiligo extent in clinical trials and in daily practice

141 Vitiligo extent is associated with increased quality-of-

142 In this study, we introduce a global Vitiligo Extent Score (VES).

143 he impact of place of birth and residence on vitiligo extent.DESIGN, SETTING, AND PARTICIPANTS A pros

144 We report a case of generalized vitiligo for which treatment with tofacitinib citrate, a

145 (h-Tyr)-reactive TCR and develop spontaneous vitiligo from an early age, we addressed the mechanism r

146 Mice with vitiligo generated 10-fold larger populations of CD8+ me

147 genome-wide association study of generalized vitiligo (GV) in non-Hispanic whites, identifying 13 con

148 Generalized vitiligo (GV) is a complex disease in which patchy depig

149 Vitiligo had a negative effect on numerous aspects and t

150 Vitiligo has a major impact on health-related quality of

151 Vitiligo has a major impact on health-related quality of

152 Vitiligo has complex immune, genetic, environmental, and

153 eruption, lichenoid reactions, pruritus, and vitiligo have been described.

154 In patients with vitiligo, higher serum levels of IL-2 correlate with low

155 the genetic architecture and pathobiology of vitiligo, highlight relationships with other autoimmune

156 Like active lesions in human vitiligo, histology of depigmenting skin reveals a patch

157 total, 301patients completed 35-item of the Vitiligo Impact Patient scale (VIPs) of who 235 were of

158 otal, 301 patients completed 35 items of the Vitiligo Impact Patient scale, of whom 235 were of skin

159 Vitiligo Impact Patient scale-Fair Skin and Vitiligo Impact Patient scale-Dark Skin versus the Short

160 efficients and Bland and Altman plots of the Vitiligo Impact Patient scale-Fair Skin and Vitiligo Imp

161 associated with a higher risk of developing vitiligo in a population of white women.

162 individuals, regardless of SSV or segmental vitiligo in association with NSV after reduction of epid

163 responses are pivotal to the development of vitiligo in disease-prone mice, and that a quantitative

164 of rapamycin induced a lasting remission of vitiligo in mice treated at the onset of disease, or in

165 or response with regard to the occurrence of vitiligo in patients receiving pembrolizumab therapy.

166 in the melanocortin system in patients with vitiligo, including decreased circulating and lesional s

167 the development of newer topical agents for vitiligo, including topical calcineurin inhibitors; new

168 Awareness of vitiligo induction in patients with melanoma is importan

169 The clinical assessment of vitiligo involves an estimation of the affected body sur

170 Vitiligo is a CD8 T cell-mediated autoimmune disease tha

171 Generalized vitiligo is a common autoimmune disease in which acquire

172 Vitiligo is a common autoimmune disease of the skin that

173 Vitiligo is a common chronic skin disorder characterized

174 Vitiligo is a common condition that is often emotionally

175 Chemical-induced vitiligo is a unique clinical presentation that reflects

176 Vitiligo is an autoimmune disease in which depigmented s

177 Vitiligo is an autoimmune disease of the skin causing di

178 Vitiligo is an autoimmune disease of the skin characteri

179 Vitiligo is an autoimmune disease of the skin in which m

180 Vitiligo is an autoimmune disease of the skin that resul

181 Vitiligo is an autoimmune skin disorder that reacts agai

182 The onset of vitiligo is associated with a greater increase in the pe

183 Vitiligo is characterized by a mostly progressive loss o

184 Vitiligo is characterized by a progressive loss of inher

185 Vitiligo is characterized by death or functional defects

186 Vitiligo is characterized by depigmented patches of skin

187 Vitiligo is characterized by depigmented skin patches ca

188 Vitiligo is clinically characterised by the development

189 Generalized nonsegmental vitiligo is often associated with the activation of mela

190 Autoimmune vitiligo is strongly associated with the MHC class II re

191 Vitiligo is the most common cutaneous depigmentation dis

192 ative stress driven, and melanocyte death in vitiligo is thought to be instigated by a highly pro-oxi

193 Generalized vitiligo is thought to have an autoimmune etiology and h

194 Moreover, different distributions of vitiligo lesions are associated with impairment of diffe

195 ratio, 1.94 [95% CI, 1.44-2.61; P<.001]) and vitiligo lesions in the genital area (1.82 [1.30-2.53; P

196 hallmark of melanocytes at the periphery of vitiligo lesions is dilation of the endoplasmic reticulu

197 ocalized with T cells, particularly in early vitiligo lesions.

198 Body surface area (BSA) of vitiligo lesions.RESULTS Patients with vitiligo who were

199 during active SLV, and decreased to near pre-vitiligo levels after complete loss of melanocytes.

200 ary estimates of the cumulative incidence of vitiligo-like depigmentation across studies.

201 apy to determine the cumulative incidence of vitiligo-like depigmentation and the prognostic value of

202 Vitiligo-like depigmentation in patients with melanoma m

203 The prognostic value of vitiligo-like depigmentation on survival outcome was ass

204 cells from the epidermis, and development of vitiligo-like lesions.

205 gher odds of AD in patients with early-onset vitiligo (<12 years) compared with those with late-onset

206 One weakness in vitiligo management is the lack of an assessment method

207 We also found in vitiligo melanocyrtes hyper-activation of the PGC1alpha

208 fically HLA-A*02:01, which presents multiple vitiligo melanocyte autoantigens.

209 examined chemotactic signatures in cultured vitiligo melanocytes and skin samples of early (</=2 mon

210 Jian et al. show that vitiligo melanocytes have impaired nuclear factor erythr

211 scent phenotype diminishes the capability of vitiligo melanocytes to cope with stressful stimuli.

212 We found in cultured epidermal vitiligo melanocytes, compared to healthy ones, low ATP,

213 immune targeting and the relationships among vitiligo, melanoma, and eye, skin and hair coloration.

214 Here, we fine-map vitiligo MHC class II genetic risk to three SNPs only 47

215 ng asthma, Crohn's disease, coeliac disease, vitiligo, multiple sclerosis and type 1 diabetes.

216 udies that included control patients without vitiligo (n = 2) and control patients without AA (n = 3)

217 llitus (n = 4), thyroid disease (n = 2), and vitiligo (n = 2).

218 Nonsegmental vitiligo (NSV) is characterized by loss of inherited ski

219 ed risk factors and regional differences for vitiligo.OBJECTIVE To determine the impact of place of b

220 Correlation between vitiligo occurrence and overall survival was also estima

221 Although vitiligo occurs only in a low percentage of patients wit

222 Oxidative stress may have a role in vitiligo onset, while autoimmunity contributes to diseas

223 ated IgG level (P = .02) as risk factors for vitiligo or AA.

224 priming of naive T cells is not required for vitiligo or its associated antitumor immunity.

225 eveloping AA (OR 1.80, 95% CI 1.18-2.76) and vitiligo (OR 2.14, 95% CI 1.29-3.54) in multivariate mod

226 2 years) compared with those with late-onset vitiligo (OR, 3.54; 95% CI, 2.24-5.63, P < .001).

227 ncident cases of AA and 98 incident cases of vitiligo over 2 years of follow-up.

228 We documented 271 cases of incident vitiligo over 835,594 person-years.

229 s difficult to determine disease activity in vitiligo owing to the absence of inflammatory signs, suc

230 001]) and number of body parts affected with vitiligo (P</=.009) but not laterality (P=.06) or durati

231 o oxidative stress is known to contribute to vitiligo pathogenesis.

232 ing skin occurred in a sizable percentage of vitiligo patients (35.1%) and were predicted by an affec

233 man leukocyte antigen (HLA) alleles in 1,404 vitiligo patients and 902 unaffected controls from North

234 n the Treg population may be therapeutic for vitiligo patients with active disease.

235 ne CXCL10 is expressed in lesional skin from vitiligo patients, and that it is critical for the progr

236 athways are dysregulated in melanocytes from vitiligo patients, suggesting that melanocyte-intrinsic

237 cell line PIG3V and skin biopsy samples from vitiligo patients, whereas its predicted targets PPARGC1

238 f vitiligo age of onset in 1,339 generalized vitiligo patients, with replication in an independent co

239 me-wide association study of 2,853 Caucasian vitiligo patients.

240 alized and localized vitiligo and in several vitiligo populations studied previously suggests that it

241 Melanocytes in patients with vitiligo possess intrinsic abnormalities that contribute

242 atological diseases such as alopecia areata, vitiligo, psoriasis and atopic dermatitis, common varian

243 The time to onset of vitiligo ranged from 52 to 453 (median, 126) days from t

244 nt of lung cancer (LC), in opposition to the vitiligo reactions that develop during melanoma treatmen

245 Although the precise mechanisms that trigger vitiligo remain elusive, autoimmune responses mediate it

246 Vitiligo repigmentation is a complex process in which th

247 The strongest stimulus for vitiligo repigmentation is narrow-band UVB (NBUVB), but

248 vation of bulge melanocyte precursors during vitiligo repigmentation.

249 epletion of CD4 T cells during the course of vitiligo rescues the priming of naive pmel T cells that

250 ith a number of human pathologies, including vitiligo, rheumatoid arthritis, and Crohn disease.

251 Vitiligo risk associated with the MHC class I region thu

252 Refined genetic mapping localizes vitiligo risk in the HLA-A region to an SNP haplotype ap

253 Additionally, vitiligo risk was higher among women with better tanning

254 Vitiligo risk was higher in women who had at least one m

255 : "psoriasis," "atopic dermatitis," "acne," "vitiligo," "seborrheic dermatitis," "alopecia areata," a

256 antitative real-time-PCR using NBUVB-treated vitiligo skin and untreated normal skin.

257 ed and narrow band UVB (NBUVB)-treated human vitiligo skin.

258 e epidermal melanocytes of the NBUVB-treated vitiligo skin.

259 ure epidermal melanocytes from NBUVB-treated vitiligo skin.

260 In SL vitiligo (SLV), postnatal loss of melanocytes in feather

261 Although a few vitiligo specific QOL instruments exist, there is no spe

262 Although a few vitiligo-specific quality of life instruments exist, the

263 Patients with uveal melanoma can develop vitiligo spontaneously or following vaccine therapy.

264 Strictly segmental vitiligo (SSV) with dermatomal distribution is a rare en

265 of these chemotactic axes as a strategy for vitiligo stabilization.

266 in the understanding of the pathogenesis of vitiligo suggest that Janus kinase inhibitors may be a t

267 Genetic studies in vitiligo support a role for stress, innate immunity, and

268 Most vitiligo susceptibility loci encode immunoregulatory pro

269 studies (GWAS1 and GWAS2), we identified 27 vitiligo susceptibility loci in patients of European anc

270 To identify generalized vitiligo susceptibility loci, we conducted a genomewide

271 differing roles played by genes involved in vitiligo susceptibility versus vitiligo age of onset, an

272 Previous genetic analyses have focused on vitiligo susceptibility, and have identified a number of

273 ion that is also associated with generalized vitiligo susceptibility.

274 MHC or non-MHC loci that are associated with vitiligo susceptibility.

275 eutralization led to increased occurrence of vitiligo that correlated with a decreased incidence of m

276 VI and a confirmed diagnosis of nonsegmental vitiligo that involved 15% to 50% of total body surface

277 mouse HSCs developed spontaneous autoimmune vitiligo that was associated with the presence of a Th1-

278 well recognised: segmental and non-segmental vitiligo (the commonest form).

279 In vitiligo, the autoimmune destruction of epidermal melano

280 In the present study we have found that vitiligo, the autoimmune destruction of melanocytes, gen

281 Vitiligo, the most common depigmenting disorder, is caus

282 The relationship of vitiligo to cutaneous melanoma is believed to be due to

283 knowledge can be harnessed for melanoma and vitiligo treatment.

284 ssential for designing better treatments for vitiligo, ultimately based on melanocyte stem cell activ

285 eveloped an adoptive transfer mouse model of vitiligo using melanocyte-specific CD8(+) T cells, which

286 About half of all vitiligo vulgaris patients have onset of their illness d

287 es in the understanding and the treatment of vitiligo vulgaris.

288 The overall cumulative incidence of vitiligo was 3.4% (95% CI, 2.5% to 4.5%).

289 terval from initial presentation to onset of vitiligo was 77 months (range, 5-168 months).

290 Vitiligo was stable or slowly progressive for 3 months.

291 genome-wide association study of generalized vitiligo, we identified ten confirmed susceptibility loc

292 nts treated with pembrolizumab who developed vitiligo were alive at the time of analysis, with a medi

293 The DLQI scores in vitiligo were associated with an affected BSA of more th

294 Ninety-three patients with vitiligo were enrolled, including 83 individuals with no

295 to eradicate melanoma and induce autoimmune vitiligo when infused into mice.

296 inary results of 4 patients with generalized vitiligo who developed repigmentation using afamelanotid

297 A) of vitiligo lesions.RESULTS Patients with vitiligo who were born outside the United States had low

298 nding of the profound psychosocial effect of vitiligo will be emphasised throughout this Seminar.

299 The association of vitiligo with tumor response in patients with melanoma w

300 served replicated association of generalized vitiligo with variants at 3p13 encompassing FOXP1 (rs170