ライフサイエンスコーパス: skin inflammation

1 how loss of TSG-6 affects wound closure and skin inflammation.

2 ulf the intact granules exocytosed by MCs on skin inflammation.

3 fective new therapeutic approach in allergic skin inflammation.

4 teolysis products from keratinocytes promote skin inflammation.

5 required for the development of spontaneous skin inflammation.

6 ermis and showed macroscopic signs of severe skin inflammation.

7 s IL-23R and IL-17 outside the thymus during skin inflammation.

8 c conditions in a mouse model of spontaneous skin inflammation.

9 ensable for the development of AD-associated skin inflammation.

10 ra(-/-) ) resulted in severe exacerbation of skin inflammation.

11 ting the systemic response in psoriasis-like skin inflammation.

12 nd results in an IL-17-linked psoriasis-like skin inflammation.

13 ng component in the pathogenesis of allergic skin inflammation.

14 i-inflammatory activity in acute and chronic skin inflammation.

15 ratinocytes and in different mouse models of skin inflammation.

16 s sufficient for mediating S. aureus-induced skin inflammation.

17 the imiquimod-induced model of psoriasiform skin inflammation.

18 L-17A-induced chronic atopic dermatitis-like skin inflammation.

19 nders those cells ineffectual in suppressing skin inflammation.

20 strated that cellular dysregulation precedes skin inflammation.

21 that is emerging as an important mediator of skin inflammation.

22 uced leukocyte recruitment and the resulting skin inflammation.

23 that this effect is associated with reduced skin inflammation.

24 resistance and the subsequent development of skin inflammation.

25 th TSLP and IL-23 expression and ameliorates skin inflammation.

26 f beneficial AHR signaling in the context of skin inflammation.

27 with blocking antibodies to CD1a alleviated skin inflammation.

28 tratum corneum, particularly during times of skin inflammation.

29 tration in a mouse model of a psoriasis-like skin inflammation.

30 kin homeostasis and prevented development of skin inflammation.

31 completely reversed dysbiosis and eliminated skin inflammation.

32 ts a molecular sensor triggering HFD-induced skin inflammation.

33 l of targeting these cells in the context of skin inflammation.

34 ry phenotype that results in increased local skin inflammation.

35 d caused epidermal hyperplasia and psoriatic skin inflammation.

36 f IkappaBzeta siRNA abolished psoriasis-like skin inflammation.

37 the cytokines IFN-gamma- and IL-17-mediated skin inflammation.

38 in TNFalpha- and IL-17 pathways in psoriatic skin inflammation.

39 emic autoimmunity characterized by prominent skin inflammation.

40 ying a new mechanism that may be involved in skin inflammation.

41 are key mediators of cathelicidin-initiated skin inflammation.

42 ng a resource for the further study of human skin inflammation.

43 be involved in activation and regulation of skin inflammation.

44 he mechanisms through which thymol can alter skin inflammation.

45 ng gammadeltaT cells have a critical role in skin inflammation.

46 -gamma-producing cells in chemically induced skin inflammation.

47 -1RI signalling have significantly decreased skin inflammation.

48 o the pathologic findings in T cell-mediated skin inflammation.

49 depletion of NKT cells abolished TPA-induced skin inflammation.

50 1 in DC trafficking and in the initiation of skin inflammation.

51 s response is important in multiple forms of skin inflammation.

52 ls and developed spontaneous IL-22-dependent skin inflammation.

53 iseases that are characterized by muscle and skin inflammation.

54 ction of TNF, IL-23, IL-17, and IL-22 during skin inflammation.

55 ere dispensable for the development of local skin inflammation.

56 d is associated with severe itch and chronic skin inflammation.

57 on of siTNFalpha shows synergism in treating skin inflammation.

58 the hyperkeratosis and fibrosis of allergic skin inflammation.

59 B4-BLT1 interaction is required for allergic skin inflammation.

60 cytes induces ZBP1-dependent necroptosis and skin inflammation.

61 relationship between the circadian clock and skin inflammation.

62 Psoriasis (PS) is a chronic skin inflammation.

63 genetic protein (BMP) signaling in psoriatic skin inflammation.

64 skin sites when studying the development of skin inflammation.

65 the controlled release of the FLUO to reduce skin inflammation.

66 ive therapy for both LL-37-and KLK-5-induced skin inflammation.

67 that DOPG could be used to inhibit excessive skin inflammation.

68 Aldara (5% imiquimod)-induced psoriasis-like skin inflammation.

69 therapeutics for controlling itch and atopic skin inflammation.

70 valents supporting a role for this target in skin inflammation.

71 tty acids (PUFAs) has potential benefits for skin inflammation.

72 keratinocytes is essential to an IMQ-induced skin inflammation.

73 regulate keratinocyte function and suppress skin inflammation.

74 n and were recently shown to limit psoriatic skin inflammation.

75 exocytosed mast cell granules (MCGs) during skin inflammation.

76 erentiation and proliferation, and regulates skin inflammation.

77 lecule, N-WASP, display cyclic hair loss and skin inflammation.

78 L-1 signaling, and recruit cells involved in skin inflammation.

79 E138A) psoriasis-associated mutation induces skin inflammation, a knock-in mouse strain was generated

80 rmed DeltaNC16A), which develops spontaneous skin inflammation accompanied by an influx of myeloid de

81 ith increased TEWL, epidermal thickness, and skin inflammation, all of which were attenuated in the a

82 T FINDINGS: It is becoming apparent that the skin inflammation alone has implications for systemic an

83 strant, cholestyramine, prevented WD-induced skin inflammation along with a reduction in the infiltra

84 ruption was not sufficient to drive allergic skin inflammation, although it did promote systemic immu

85 T cells (Tregs) are important in controlling skin inflammation, an effect dependent on their ability

86 TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in A

87 sion of CARD14(E138A) induced more extensive skin inflammation and a severe systemic disease involvin

88 y response in the imiquimod-induced model of skin inflammation and AhR-deficient mice exhibited a sub

89 our data indicate that omalizumab can induce skin inflammation and anaphylaxis by engaging FcgammaRs,

90 d between omalizumab and IgE can induce both skin inflammation and anaphylaxis through engagement of

91 notypes and endotypes that result in chronic skin inflammation and barrier dysfunction are modified b

92 Crisaborole reversed biomarker profiles of skin inflammation and barrier function, with associated

93 Tacrolimus treatment reduced skin inflammation and blocked cancer development in MRL/

94 icant reactions are accompanied by localized skin inflammation and concomitant increases in site-spec

95 henotype was associated with chronic sterile skin inflammation and could be partially rescued by dexa

96 howed decreased IL-23-induced psoriasis-like skin inflammation and cytokine gene expression, consiste

97 and -11 from cpdm mice significantly reduced skin inflammation and delayed disease onset, whereas sys

98 oriasis patients experience chronic systemic skin inflammation and develop cardiovascular comorbiditi

99 sferable to naive animals, where it augments skin inflammation and disease severity.

100 ciency attenuated IMQ-induced psoriasis-like skin inflammation and enhanced IMQ-induced parakeratosis

101 IL-1 signaling, which is sufficient to cause skin inflammation and epidermal hyperplasia.

102 ck Langerhans cells (LC) developed increased skin inflammation and expressed higher amounts of IL-6,

103 t that LIGHT may be an important mediator of skin inflammation and fibrosis in diseases such as scler

104 This was essential to induce skin inflammation and for the recruitment of pDCs to the

105 Sensitized mice show more rapid skin inflammation and greater proliferation and IL-17 pr

106 eficient and CCR6-deficient mice had reduced skin inflammation and IL-17A expression.

107 arious preclinical models of lung, bowel and skin inflammation and ischaemia-reperfusion injury relev

108 anti-gammadeltaTCR Abs significantly reduced skin inflammation and largely eliminated pathological ga

109 epicutaneous Staphylococcus aureus promotes skin inflammation and may contribute to AD.

110 erstanding of the central role of the AhR in skin inflammation and may point toward a potential role

111 ts with murine models of allergic airway and skin inflammation and offer an overview of studies focus

112 entiate cellular defense against UVB-induced skin inflammation and photocarcinogenesis through elevat

113 acids (PUFAs) on ultraviolet B (UVB)-induced skin inflammation and photocarcinogenesis using hairless

114 ta-IL-1R signaling pathway may contribute to skin inflammation and psoriasis pathogenesis via the dir

115 ession of dermatitis, as revealed by reduced skin inflammation and reduced serum IgE levels in mice l

116 ion resulting in significant amelioration of skin inflammation and reductions in skin-infiltrating pa

117 skin microbiota, respectively, resolved the skin inflammation and restored keratinocyte intracellula

118 omotes AD-associated itch independently from skin inflammation and reveal a previously unrecognized e

119 ermally to be effective, which causes severe skin inflammation and sometimes, permanent scars.

120 These findings identify a role for IL-17C in skin inflammation and suggest a pathogenic function for

121 itochondrial respiratory chain complexes and skin inflammation and suggest that severe respiratory ch

122 ntribution of Mon/Mac cells in IL-23 related skin inflammation and suggest that these cells are a sig

123 h of which signals through IL-1R, instigates skin inflammation and systemic disease is not known.

124 CARD14(E138A)-induced skin inflammation and systemic disease were independent

125 Factors that determine the presence of skin inflammation and the joint arthritis susceptibility

126 old mice with severe skin disease eliminated skin inflammation and the presence of aortic root lesion

127 bited T(FH)/GC response and suppressed T(H)2 skin inflammation and the subsequent asthma.

128 l numbers strongly increase during psoriatic skin inflammation and were recently shown to limit psori

129 Smad7 below an oncogenic level to alleviate skin inflammation and wound healing defects associated w

130 We assessed the roles of Smad7 in skin inflammation and wound healing using genetic and ph

131 d IL-17C drive the pathogenesis of psoriatic skin inflammation, and anti-IL-17A Abs were recently app

132 n for the intervention, the role of managing skin inflammation, and differences between primary and s

133 e, a model for IL-17A-induced psoriasis-like skin inflammation, and flaky-tail (Flg (ft) ) mice, a mo

134 in an imiquimod cream-induced mouse model of skin inflammation, and it reduces airway inflammation in

135 of iRhom2 are discussed with respect to the skin, inflammation, and the antiviral response.

136 s in IL1r(-/-) mice was associated with less skin inflammation as characterized by decreased recruitm

137 nsity of IgE autoreactivity seemed to follow skin inflammation as it was reduced during full-dose tre

138 IL-1Ra1 deficiency aggravated Aldara-induced skin inflammation, as demonstrated by increased ear thic

139 TRPV1 but not TRPA1 channels protect the skin inflammation, as genetic ablation of TRPV1 function

140 of Ccr4(+) splenic T cells and worsening of skin inflammation, as indicated by epidermal thickening,

141 ith reported side effects ranging from local skin inflammation at the injection site to systemic anap

142 to T helper type 1-/T helper type 17-biased skin inflammation before significant body weight gain.

143 nockout mice were resistant to IL-23-induced skin inflammation but exhibited no changes in joint infl

144 t severe psoriasis involves higher levels of skin inflammation, but comparative molecular profiles of

145 atively, neonatal mice did not develop overt skin inflammation, but exhibited systemic release of IL-

146 iciency (Zc3h12a(+/-)) displayed no baseline skin inflammation, but they showed exacerbated pathology

147 ociceptors drive the development of allergic skin inflammation by inducing the degranulation of mast

148 ults show that topical IVM improved allergic skin inflammation by reducing the priming and activation

149 bone marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cr

150 To investigate whether allergic skin inflammation can also facilitate priming toward new

151 Upon induction of skin inflammation, CD11b(+) dDC in IRF4(-/-) mice did no

152 /- mice spontaneously developed psoriasiform skin inflammation characterized by T cell and neutrophil

153 te allotransplantation can trigger localized skin inflammation consistent with rejection.

154 During initial stages of skin inflammation, DCs dynamically scan MCs, whereas at

155 e skin leads to amelioration of psoriasiform skin inflammation, decreased epidermal proliferation, an

156 Overall, skin inflammation, defined as the sum of T-cell infiltra

157 ived lipid urushiol triggered CD1a-dependent skin inflammation driven by CD4(+) helper T cells that p

158 sA, it remains unclear whether IL-23-induced skin inflammation drives joint disease.

159 Here we show, in mice, that skin inflammation enhances levels of IgE antibodies that

160 sis and in a mouse model of a psoriasis-like skin inflammation, epidermal vaspin expression was signi

161 itization led to a considerable reduction of skin inflammation, even when rechallenged up to 3 wk aft

162 which 70% of patients experience disfiguring skin inflammation (grouped under the rubric of cutaneous

163 harmaceuticals, St. Paul, MN) model of acute skin inflammation has become the most widely used mouse

164 Using two mouse models of ear skin inflammation (histamine- and IgE-mediated passive c

165 IFN-gamma mediates chemically induced skin inflammation; however, the mechanism by which IFN-g

166 IL-17C+KO mice initially exhibited decreased skin inflammation; however, this decrease was transient

167 implicated in severe pruritus during atopic skin inflammation, IL-31's neuropoietic potential remain

168 IL-1beta levels contribute to development of skin inflammation in a mouse model of injury-induced ski

169 y was to investigate the role of miR-146a in skin inflammation in AD.

170 atory responses in keratinocytes and chronic skin inflammation in AD.

171 ion with S. aureus can contribute to chronic skin inflammation in AD.

172 ht contribute to the aggravation of allergic skin inflammation in AD.

173 tapinarof has no impact on imiquimod-induced skin inflammation in AhR-deficient mice.

174 cellular pathways associated with increased skin inflammation in all 3 conditions and presents mecha

175 ency in XBP1 attenuated IL-23 expression and skin inflammation in an IL-23-dependent model of psorias

176 Chronic skin inflammation in atopic dermatitis (AD) is associate

177 (2) (PGD(2)), a lipid mediator that promotes skin inflammation in atopic dermatitis (AD).

178 Administration of CCX2553 ameliorated skin inflammation in both the IL-23-induced ear swelling

179 intervention strategies designed to mitigate skin inflammation in children with AD.

180 Although skin inflammation in cpdm mice is driven by TNF- and RIP

181 l pathogenic similarities between muscle and skin inflammation in dermatomyositis.

182 ate how best to manage all manifestations of skin inflammation in dermatomyositis.

183 strated by the development of intestinal and skin inflammation in diseases caused by primary deficien

184 ylococcus aureus colonization contributes to skin inflammation in diseases such as atopic dermatitis,

185 To understand the mechanisms of persistent skin inflammation in DOCK8 deficiency, we examined mice

186 ting Treg function may be useful in treating skin inflammation in DOCK8 deficiency.

187 role of water hardness in the initiation of skin inflammation in early life, but there is a need for

188 determine the immunologic rules that govern skin inflammation in early life.

189 lammation in a mouse model of injury-induced skin inflammation in filaggrin-deficient mice without th

190 From June 28-30, 2018, a course entitled "Skin Inflammation in Human Health and Disease: 2018 Inte

191 The barrier dysregulation and spontaneous skin inflammation in Il17ra(-/-) mice was dependent on T

192 Cs and Treg cells; and modeling of psoriatic skin inflammation in mice lacking the BMPR type 1a in CD

193 sing RIPK1 with mutated RHIM (Ripk1(mR/mR)), skin inflammation in mice with epidermis-specific RIPK1

194 ro, disrupt the physical barrier, and induce skin inflammation in mice.

195 etradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was exam

196 ment of the LC network preceding spontaneous skin inflammation in mutant mice that lack all three TAM

197 erplay between gut and skin that can sustain skin inflammation in OS.

198 and whether they contribute to the aberrant skin inflammation in patients with AD is unknown.

199 promising therapeutic option for controlling skin inflammation in patients with peeling skin syndrome

200 king non-cell-autonomous EBER1 presence with skin inflammation in predisposed individuals.

201 that overexpression of miR-31 contributes to skin inflammation in psoriasis lesions by regulating the

202 LukGH or PVL caused skin inflammation in rabbits and a monkey, but deletion

203 d that Trim32 null mice developed Th2-biased skin inflammation in response to imiquimod and associate

204 ls are depleted in wild-type mice developing skin inflammation in response to immunization or contact

205 PRAS40(T246A) mice also displayed attenuated skin inflammation in response to TPA.

206 Furthermore, skin inflammation in Sharpin(cpdm) mice is specifically

207 and IL-1R signaling are required to provoke skin inflammation in Sharpin(cpdm) mice.

208 signaling in epidermal keratinocytes drives skin inflammation in Sharpin-deficient mice.

209 etradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in these mutant mice, whereas it was c

210 ingly critical role for IFNs in evolution of skin inflammation in these patients has been recognized.

211 n CD8 T-cell activation and functions during skin inflammation in vitro and in vivo and examined the

212 ismutase 3 (SOD3) on LL-37- or KLK-5-induced skin inflammation in vitro and in vivo and its underlyin

213 IL-1alpha was necessary and sufficient for skin inflammation in vivo and secreted from keratinocyte

214 dendritic cell/IL-15-mediated, T cell-driven skin inflammation in vivo, and is relevant to human psor

215 Anti-IL-17A treatment ameliorated skin inflammation in vivo.

216 in acute murine IL-23- and imiquimod-induced skin inflammation, in human psoriasis is still unclear.

217 mising therapeutic target in T cell-mediated skin inflammation, including psoriasis.

218 that C3 drives tumorigenesis during chronic skin inflammation, independently of the downstream gener

219 reactions and imiquimod-triggered psoriatic skin inflammation, indicating that E-cadherin on LC does

220 allergen is effective in preventing allergic skin inflammation induced by biting midge.

221 We produced models of skin inflammation induced by imiquimod (IMQ) and IL-23 a

222 expression, and acanthosis in psoriasis-like skin inflammation induced by imiquimod.

223 6 dysregulation in a mouse model, we studied skin inflammation induced by intradermal injections of p

224 MCs protect from the exacerbated allergic skin inflammation induced by repeated allergen challenge

225 The compound also significantly suppressed skin inflammation induced by topical administration of t

226 MCGs in vivo, we tracked the MCG fate after skin inflammation-induced MC degranulation.

227 -/- mice expressing RAS blocked CD8-mediated skin inflammation, inducible nitric oxide synthase expre

228 osure to mouse skin promoted MyD88-dependent skin inflammation initiated by IL-36, but not IL-1alpha/

229 Skin injury of ft/ft mice induced chronic skin inflammation involving dysbiosis-driven intracellul

230 ich S. aureus epicutaneous exposure promotes skin inflammation involving IL-36R/MyD88-dependent IL-17

231 a challenge because the development of local skin inflammation is often unavoidable.

232 Even without the alleviation of skin inflammation, KLK7-deficient mice exhibited signifi

233 These findings establish that local skin inflammation leads to faster and stronger secondary

234 sis and suggest that aggressive treatment of skin inflammation may attenuate pro-inflammatory and pro

235 Skin inflammation measured as Psoriasis Area and Severit

236 These diseases are characterized by skin inflammation mediated by activated innate immunity

237 useful immunosuppressive strategy to control skin inflammation mediated by the IL-23/IL-1beta/IL-17 a

238 In TPA-induced skin inflammation, MIF is released from damaged keratino

239 to prevent AD or to aggressively treat early skin inflammation might modify the risk of mental health

240 oward new antigens, we developed an allergic skin inflammation model based on an allergic lung inflam

241 Further, in an acute skin inflammation model, LCN-2-knockout mice exhibited a

242 ata from a novel mouse model of psoriasiform skin inflammation not only highlight the importance of t

243 rmal link between genetic predisposition and skin inflammation observed in HS.

244 phora occurred in 24 versus five, and eyelid skin inflammation occurred in seven versus none.

245 Strikingly, skin inflammation occurs independently of adaptive immun

246 Allergic skin inflammation often presents in early childhood; how

247 This decrease in skin inflammation paralleled decreases in splenic neutro

248 at miR-146a-mediated suppression in allergic skin inflammation partially occurs through direct target

249 factor in the initiation and exacerbation of skin inflammation, particularly in patients with atopic

250 cal inhibition of Duox1 completely abrogated skin inflammation, placing Duox1-derived H(2)O(2) upstre

251 Importantly, chronic skin inflammation promoted the massive accumulation of I

252 recently been demonstrated that neutrophilic skin inflammation promotes angiotropism and metastatic s

253 Our study suggests that skin inflammation reduces the expression of FLG-like pro

254 ular mechanisms that regulate psoriasis-like skin inflammation remain to be fully understood.

255 The expression of GITRL in skin inflammation remains unknown.

256 eutics within the epidermis can safely treat skin inflammation, scaling, and erythema associated with

257 A demethylation within a minimal promoter in skin/inflammation-seeking effector memory T cells.

258 Skin inflammation significantly improved in KC-Tie2 mice

259 TSLP), previously shown to be induced during skin inflammation, stimulates myeloid-related BDCA-11 pe

260 kin is a common feature of acute and chronic skin inflammation such as psoriasis and contact or atopi

261 The mechanisms leading to allergic skin inflammation, such as atopic dermatitis or urticari

262 ) mice revealed a similar degree of allergic skin inflammation, systemic atopy, and airway hypersensi

263 310 SUMOylation site, revealed a more severe skin inflammation than in WT mice.

264 loped more frequent and more severe allergic skin inflammation than Stat6VT transgenic mice that had

265 Atopic dermatitis (AD) is a chronic skin inflammation that affects children and adults world

266 itization in mice results in T(H)2-dominated skin inflammation that mimics atopic dermatitis and sens

267 ratinocyte proliferation in a mouse model of skin inflammation that shares many features of AD.

268 apoptosis and necroptosis and caused severe skin inflammation that was prevented by RIPK3 but not FA

269 9 was genetically deleted in mouse models of skin inflammation, the psoriasis-like skin disease and i

270 Skin inflammation; thrombosis clotting times; and percen

271 is a potent negative regulator of psoriatic skin inflammation through IL-17A and IL-17C.

272 CD4(+) effector T cells to transfer allergic skin inflammation to Ltb4r1(-/-) recipients.

273 tudy we have developed a model of autoimmune skin inflammation, to determine key parameters in the ge

274 nstrates how the epidermis triggers unwanted skin inflammation under disease conditions.

275 antigen-specific Tregs and does not prevent skin inflammation upon later-life exposure.

276 acrophage metabolism and polarization and in skin inflammation using a model of imiquimod-induced pso

277 ccumulation, we developed a simple system of skin inflammation using defined Ags and adjuvants that i

278 cate that IL-36 cytokines actively propagate skin inflammation via the activation of keratinocytes, A

279 We found that exaggerated skin inflammation was absent in DeltaLC x CXCR6(-/-) mic

280 Skin inflammation was assessed by SCORAD.

281 found that imiquimod-induced psoriasis-like skin inflammation was completely absent in IkappaBzeta-d

282 The severity of psoriasis-like skin inflammation was evaluated at morphologic, histolog

283 icient ft/ft mice was performed, and ensuing skin inflammation was evaluated by using digital photogr

284 The associated skin inflammation was mediated by IL-5-expressing pathog

285 of histone deacetylase-3 (HDAC3) in allergic skin inflammation was reported.

286 bsent in IkappaBzeta-deficient mice, whereas skin inflammation was still inducible in IL-17A- and TNF

287 an experimental mouse model of psoriasiform skin inflammation, we demonstrate in vivo connections be

288 quimod-induced psoriasis-like mouse model of skin inflammation, we explored the role of IL-1 signalin

289 se these cytokines are crucially involved in skin inflammation, we hypothesize that IL-31-specific ac

290 role of IL-22BP in controlling IL-22 during skin inflammation, we used imiquimod-induced skin diseas

291 PAPA syndrome such as pyogenic arthritis and skin inflammation were not recapitulated in the mouse mo

292 Ag-specific Teff cells resulted in enhanced skin inflammation when compared with CD27-deficient Teff

293 release that was sufficient to drive chronic skin inflammation, which has implications for AD pathoge

294 signaling, IL-22 was the main contributor to skin inflammation, which provides a molecular mechanism

295 pha-toxin or delta-toxin, contributed to the skin inflammation, which was driven by IL-17-producing g

296 kinase 3 (RIPK3) deficiency fully prevented skin inflammation, while single RIPK3 deficiency only de

297 ation also developed spontaneous progressive skin inflammation with eosinophilia, as well as increase

298 KC-Tie2 mice develop psoriasiform skin inflammation with increases in IL-23 and IL-17A and

299 lts show that CD8(+) T cells can orchestrate skin inflammation with psoriasis-like pathology in respo

300 o earlier onset and exacerbated pathology of skin inflammation, with increased expression of IL-17-in