ライフサイエンスコーパス: vitiligo

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

2 -ultraviolet B in patients with nonsegmental vitiligo.

3 biomarkers and therapeutic targets in human vitiligo.

4 ation and mitochondrial energy metabolism in vitiligo.

5 0B as a potential disease activity marker in vitiligo.

6 actions to sun exposure and risk of incident vitiligo.

7 e is excitement in the air for patients with vitiligo.

8 effective treatment option for patients with vitiligo.

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

10 , which supports their role as biomarkers in vitiligo.

11 e included and screened for the emergence of vitiligo.

12 ditional subgroup of patients with extensive vitiligo.

13 oral prednisolone with improved outcomes for vitiligo.

14 nonsegmental vitiligo and 10 with segmental vitiligo.

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

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

17 ibitors may be effective in the treatment of vitiligo.

18 imvastatin may be an effective treatment for vitiligo.

19 and interfollicular epidermis of UV-treated vitiligo.

20 ance of depigmentation in our mouse model of vitiligo.

21 pidermis, which was lacking in the untreated vitiligo.

22 d, low-avidity T cells cause less autoimmune vitiligo.

23 targeted treatment option for patients with vitiligo.

24 y to support repigmentation in patients with vitiligo.

25 B) phototherapy is used extensively to treat vitiligo.

26 continental variation for rates of extensive vitiligo.

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

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

29 ddressed the mechanism regulating autoimmune vitiligo.

30 se progressive depigmentation and autoimmune vitiligo.

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

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

33 od and Drug Administration-approved drug for vitiligo.

34 t induce robust repigmentation phenotypes in vitiligo.

35 ally no remaining 'missing heritability' for vitiligo.

36 cles in AA and intraepidermal melanocytes in vitiligo.

37 UVB was shown to be effective especially in vitiligo.

38 and play a vital role for repigmentation in vitiligo.

39 ubsets is not yet available in patients with vitiligo.

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

41 or the melanocyte biology and development of vitiligo.

42 icacy and fewest adverse events for treating vitiligo?

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

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

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

46 Vitiligo, a clinically visible immune-related adverse ev

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

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

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

50 ow-effect-size risk alleles within multiplex-vitiligo-affected families.

51 Vitiligo, an acquired pigmentary disorder of unknown ori

52 Vitiligo, an autoimmune disease in which skin melanocyte

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

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

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

56 447 participants were included in the AA and vitiligo analyses, respectively.

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

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

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

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

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

62 ocus on the regenerative medicine aspects of vitiligo and AA, using experimental data from human, mou

63 Vitiligo and alopecia areata (AA) are common autoimmune

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

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

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

67 ytes are the target of immune destruction in vitiligo and are hypothesized to be the site of immune a

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

69 ulation of the epidermis with melanocytes in vitiligo and in regrowth of hair follicles in AA.

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

71 ent memory T cells (Trm) form in the skin in vitiligo and persist to maintain disease, as white spots

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

73 ential of ruxolitinib cream in patients with vitiligo and report the efficacy and safety results up t

74 skin CD8(+) T(RM) in maintaining disease in vitiligo and the opportunity to target this population t

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

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

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

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

79 ns characterized by white spots on the skin (vitiligo) and bald spots on the scalp (AA), which signif

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

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

82 hat provide insight into the pathogenesis of vitiligo, and how this insight has been utilized to crea

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

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

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

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

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

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

89 r higher improvement from baseline in facial Vitiligo Area Scoring Index (F-VASI) at week 24 were re-

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

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

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

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

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

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

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

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

98 vered the importance of autoimmune memory in vitiligo because cessation of treatment frequently led t

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

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

101 eated vitiligo bulge compared with untreated vitiligo bulge.

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

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

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

105 1000 Genomes Project data in unrelated 2812 vitiligo cases and 37 079 controls genotyped genome wide

106 Most vitiligo cases are "simplex," where there is no family h

107 risk alleles identified by GWAS in multiplex vitiligo cases relative to simplex cases.

108 disproportionately more to risk in multiplex vitiligo cases than in simplex cases, supporting a speci

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

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

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

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

113 critical regulator of cellular metabolism in vitiligo cells.

114 and respiratory responses were defective in vitiligo cells.

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

116 nd activated T-cell subsets in patients with vitiligo compared with patients with AA, AD, or psoriasi

117 we investigate whether simplex and multiplex vitiligo comprise different disease subtypes with differ

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

119 e characterization of skin memory T cells in vitiligo, demonstrate that Trm and Tcm work together dur

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

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

122 7 studies reporting individual patient data, vitiligo development was significantly associated with b

123 respectively, compared with patients without vitiligo development.

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

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

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

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

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

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

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

131 Vitiligo extent is associated with increased quality-of-

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

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

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

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

136 score, which has allowed various aspects of vitiligo genetic architecture in the EUR population to b

137 Vitiligo had a negative effect on numerous aspects and t

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

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

140 Vitiligo has an estimated prevalence of about 0.2-2% in

141 Vitiligo has complex immune, genetic, environmental, and

142 Vitiligo has thus proved to be a particularly tractable

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

144 s genome-wide association studies (GWASs) of vitiligo have identified 50 susceptibility loci.

145 s of this study were to estimate and compare vitiligo heritability in European-derived patients using

146 ese results demonstrate that essentially all vitiligo heritable risk is captured by array-based genot

147 We found that high vitiligo, high psoriasis, and low atopic dermatitis poly

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

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

150 roborated with our findings in patients with vitiligo, identified RHOJ involvement in UV response and

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

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

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

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

155 blind, phase 2 study for adult patients with vitiligo in 26 US hospitals and medical centres in 18 st

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

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

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

159 IFN-gamma signaling can effectively reverse vitiligo in humans; however, disease relapse is common a

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

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

162 Awareness of vitiligo induction in patients with melanoma is importan

163 s strongly suggest that family clustering of vitiligo involves a high burden of the same common, low-

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

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

166 Vitiligo is a chronic autoimmune disease resulting in sk

167 Vitiligo is a common autoimmune disease of the skin that

168 Vitiligo is a common chronic skin disorder characterized

169 Vitiligo is a common condition that is often emotionally

170 Vitiligo is a complex disease in which autoimmune destru

171 Autoimmune vitiligo is a complex disease involving polygenic risk f

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

173 Vitiligo is an autoimmune disease in which depigmented s

174 Vitiligo is an autoimmune disease in which melanocyte de

175 Vitiligo is an autoimmune disease of the skin characteri

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

177 Vitiligo is an autoimmune disease of the skin that resul

178 Vitiligo is an autoimmune disease of the skin that targe

179 Vitiligo is an autoimmune disease that results in patche

180 Vitiligo is an autoimmune skin disease mediated by autor

181 Vitiligo is an autoimmune skin disorder that reacts agai

182 l are a reminder that clinical management of vitiligo is challenging at best, even when combining ant

183 Vitiligo is characterized by a multicytokine polarizatio

184 Vitiligo is characterized by death or functional defects

185 Vitiligo is clinically characterised by the development

186 Vitiligo is impacted by environmental triggers.

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

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

189 Vitiligo is the most common cutaneous depigmentation dis

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

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

192 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

193 ssociated with substantial repigmentation of vitiligo lesions up to 52 weeks of treatment, and all do

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

195 ibed melanocyte-specific autoreactive Trm in vitiligo lesions.

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

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

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

199 Vitiligo-like depigmentation in patients with melanoma m

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

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

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

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

204 These findings suggest that vitiligo may provide a particularly tractable model for

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

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

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

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

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

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

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

212 Thus, for vitiligo, MHC regulatory variation confers extreme risk,

213 moderate-to-severe nonsegmental/generalized vitiligo, moderate-to-severe AA (n = 32), psoriasis (n =

214 nd recirculating memory T cells (Tcm) in our vitiligo mouse model.

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

219 Correlation between vitiligo occurrence and overall survival was also estima

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

221 ligo, though occasional family clustering of vitiligo occurs, and some "multiplex" families report nu

222 measures might promote skin health and delay vitiligo onset.

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 o oxidative stress is known to contribute to vitiligo pathogenesis.

231 ibe the presence of CD8(+) T(RM) in lesional vitiligo patient skin and suggest their role as active p

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

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

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

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

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

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

238 ed that ligands for NKG2D are upregulated in vitiligo perilesional skin and especially in patients wi

239 These have been combined into a vitiligo polygenic risk score, which has allowed various

240 ompared the performance of several different vitiligo polygenic risk scores derived from GWAS data.

241 Melanocytes in patients with vitiligo possess intrinsic abnormalities that contribute

242 4258 parents or offspring) of 2122 unrelated vitiligo probands.

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

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

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

246 timated family-based heritability (h2FAM) by vitiligo recurrence among a total 8034 first-degree rela

247 There is no approved treatment for vitiligo repigmentation and current off-label therapies

248 Vitiligo repigmentation is a complex process in which th

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

250 vation of bulge melanocyte precursors during vitiligo repigmentation.

251 Patients with vitiligo require lifelong treatment to regain and mainta

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

253 Vitiligo risk associated with the MHC class I region thu

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

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

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

257 toimmune diseases, polygenic architecture of vitiligo risk, vitiligo triggering, and disease onset, a

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

259 Vitiligo severity correlated with levels of multiple cyt

260 Patients with Vitiligo showed the highest CLA(+)/CLA(-) T(H)1/type 1 c

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

262 rs from the hair follicle bulge of untreated vitiligo skin and vitiligo skin treated with narrow-band

263 ollicle bulge of untreated vitiligo skin and vitiligo skin treated with narrow-band UVB.

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

265 ure epidermal melanocytes from NBUVB-treated vitiligo skin.

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

267 ever, provides a framework for understanding vitiligo: Skin resident CD8 T cells recognize and kill m

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

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

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

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

272 Aiming to define vitiligo subtypes, we discovered that age-of-onset is bi

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

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

275 ociated with cardio-metabolic phenotypes and Vitiligo, supporting a potential role for variable mitoc

276 and genomewide association studies, over 50 vitiligo susceptibility loci have been discovered.

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

278 ing dissection of heritability, discovery of vitiligo susceptibility loci through candidate gene, gen

279 ry T-cell counts were lower in patients with vitiligo than in control subjects and patients with AD o

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

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

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

283 In vitiligo, the autoimmune destruction of epidermal melano

284 In repigmentation of human vitiligo, the melanocyte (MC) precursors in the hair fol

285 Vitiligo, the most common depigmenting disorder, is caus

286 implex," where there is no family history of vitiligo, though occasional family clustering of vitilig

287 ranging from psoriasis to alopecia areata to vitiligo to lupus erythematosus to atopic dermatitis and

288 knowledge can be harnessed for melanoma and vitiligo treatment.

289 es, polygenic architecture of vitiligo risk, vitiligo triggering, and disease onset, and provide sugg

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

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

292 Vitiligo was stable or slowly progressive for 3 months.

293 Using biopsies from patients with vitiligo, we have selectively harvested, by laser captur

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

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

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

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

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

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

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