ライフサイエンスコーパス: skin inflammation

1 teolysis products from keratinocytes promote skin inflammation.

2 completely reversed dysbiosis and eliminated skin inflammation.

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

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

5 ry phenotype that results in increased local skin inflammation.

6 d caused epidermal hyperplasia and psoriatic skin inflammation.

7 f IkappaBzeta siRNA abolished psoriasis-like skin inflammation.

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

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

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

11 emic autoimmunity characterized by prominent skin inflammation.

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

13 are key mediators of cathelicidin-initiated skin inflammation.

14 be involved in activation and regulation of skin inflammation.

15 he mechanisms through which thymol can alter skin inflammation.

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

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

18 -1RI signalling have significantly decreased skin inflammation.

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

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

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

22 1 in DC trafficking and in the initiation of skin inflammation.

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

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

25 iseases that are characterized by muscle and skin inflammation.

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

27 ere dispensable for the development of local skin inflammation.

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

29 on of siTNFalpha shows synergism in treating skin inflammation.

30 the hyperkeratosis and fibrosis of allergic skin inflammation.

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

32 ficantly improved TGM activity and decreased skin inflammation.

33 nduce potent regulatory T cells that inhibit skin inflammation.

34 ating that IL-31 is involved in Th2-mediated skin inflammation.

35 K in mice resulted in a striking increase in skin inflammation.

36 intenance of suppression in chronic allergic skin inflammation.

37 n, barrier development, and IL-17-associated skin inflammation.

38 ily and the Th17 cytokines in the context of skin inflammation.

39 sitized to allergens in the gut promote this skin inflammation.

40 results in epidermal hyperproliferation and skin inflammation.

41 d for the development of lupus serum-induced skin inflammation.

42 Lupus serum depleted of IgG failed to cause skin inflammation.

43 and identify key factors in TGFbeta1-induced skin inflammation.

44 by which a product of staphylococci inhibits skin inflammation.

45 e TGFbeta1 in the epidermis developed severe skin inflammation.

46 a direct role for TGFbeta1 overexpression in skin inflammation.

47 nd could be a therapeutic target in allergic skin inflammation.

48 against P. acnes suppressed P. acnes-induced skin inflammation.

49 hich is important for preventing ROS-induced skin inflammation.

50 dermatitis (AD) is characterized by allergic skin inflammation.

51 ent DNA repair and a subsequent reduction in skin inflammation.

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

53 s with AD and used a mouse model of allergic skin inflammation.

54 in barrier dysfunction in eliciting allergic skin inflammation.

55 Th17 cell-dependent disease in this model of skin inflammation.

56 ntrolled IFN responses that drive autoimmune skin inflammation.

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

58 ant role in epidermal hyperproliferation and skin inflammation.

59 derstanding of its involvement in UV-induced skin inflammation.

60 ading to the suppression of allergen-induced skin inflammation.

61 tions have a pivotal role in T cell-mediated skin inflammation.

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

63 ng component in the pathogenesis of allergic skin inflammation.

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

65 ratinocytes and in different mouse models of skin inflammation.

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

67 the imiquimod-induced model of psoriasiform skin inflammation.

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

69 nders those cells ineffectual in suppressing skin inflammation.

70 strated that cellular dysregulation precedes skin inflammation.

71 required for the development of spontaneous skin inflammation.

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

73 uced leukocyte recruitment and the resulting skin inflammation.

74 resistance and the subsequent development of skin inflammation.

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

76 with blocking antibodies to CD1a alleviated skin inflammation.

77 ermis and showed macroscopic signs of severe skin inflammation.

78 tratum corneum, particularly during times of skin inflammation.

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

80 kin homeostasis and prevented development of skin inflammation.

81 nti-TSLP blocked the development of allergic skin inflammation after cutaneous antigen challenge of O

82 21R-IgG2aFc fusion protein failed to develop skin inflammation after e.c. sensitization of tape-strip

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

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

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

88 n K5.TGFbeta1(wt) mice significantly delayed skin inflammation and associated epidermal hyperplasia/h

89 cus aureus infections are known triggers for skin inflammation and can modulate immune responses.

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

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

92 sgenic mice from the development of allergic skin inflammation and decreased recovery time in barrier

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

94 Rosiglitazone attenuated bleomycin-induced skin inflammation and dermal fibrosis as well as subcuta

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

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

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

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

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

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

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

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

103 RabGEF1-deficient mice developed severe skin inflammation and had increased numbers of mast cell

104 VT) are prone to the development of allergic skin inflammation and have decreased expression of EDC g

105 and that mice lacking RabGEF1 develop severe skin inflammation and increased numbers of dermal mast c

106 consider possible mechanistic links between skin inflammation and increased risks of (1) obesity or

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

108 lator of TNF signaling in skin and regulates skin inflammation and keratinocyte death.

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

110 Neutralization of TNFalpha exacerbated skin inflammation and markedly enhanced the expression o

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

112 The mechanisms linking skin inflammation and observed defects in skin barrier f

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

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

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 n and less-well-characterized differences in skin inflammation and repair processes.

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

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

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

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

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

123 The increased UVB irradiation-mediated skin inflammation and TNF-alpha production in Xpa-/- mic

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

125 delivered gene therapy of cutaneous tumors, skin inflammation, and dominant negative genetic skin di

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

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

128 al in the development of lupus serum-induced skin inflammation, and lupus serum IgG induced monocyte

129 retreatment markedly inhibited ear swelling, skin inflammation, and production of pro-inflammatory cy

130 ells may be proximal regulators of psoriatic skin inflammation, and warrant further attention as ther

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

132 mice that develop T cell-mediated autoimmune skin inflammation as compared with MHC-matched healthy s

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

134 nstrated that TAK1 is the major regulator of skin inflammation as well as keratinocyte death in vivo.

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

136 Disease can be induced by skin inflammation but not solely by activation of T cell

137 -13 transgene expression resulted in reduced skin inflammation but with no effect on further progress

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

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

140 Evaluation of T-cell-mediated skin inflammation by assaying contact hypersensitivity i

141 However, induction of skin inflammation by one topical application of DNFB fol

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

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

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

145 lipid radical and nitrotyrosine early in the skin inflammation caused by LPS.

146 Skin inflammation causes innocuous heat to become painfu

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

148 over, the Nlrp3 gene-targeted mice exhibited skin inflammation characterized by neutrophil infiltrati

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

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

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

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

153 Allergic skin inflammation developed in the WT mice but not in th

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

155 yte-specific deletion of Tak1 exhibit severe skin inflammation due to hypersensitivity to tumor necro

156 lockade of LTB4 synthesis inhibited allergic skin inflammation elicited by cutaneous antigen challeng

157 Allergic skin inflammation elicited by epicutaneous immunization

158 ated with VV at sites of Th2-biased allergic skin inflammation elicited by epicutaneous ovalbumin (OV

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

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

161 Furthermore, they report that not only does skin inflammation exacerbate LN-directed Treg homing, it

162 to determine the ability of RDP58 to inhibit skin inflammation following exposure to the well-charact

163 om SLE patients and lupus-prone mice induces skin inflammation following intradermal injection into n

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

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

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

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

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

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 Chronic skin inflammation in atopic dermatitis (AD) is associate

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

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

178 acid (TNBS-colitis), as well as colitis and skin inflammation in C57BL/10 RAG-2(-/-) mice reconstitu

179 se from keratinocytes and caused exacerbated skin inflammation in CD39-/- mice.

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

181 ed in increased PAF-R agonistic activity and skin inflammation in comparison with control mice.

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

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

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

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

186 tic alternative for targeting Th1/Th2-driven skin inflammation in experimental AD.

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

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

189 ng TNFalpha blockade-induced exacerbation of skin inflammation in murine psoriasis-like skin disease.

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

191 ding to dysregulated IL-1beta production and skin inflammation in neonatal mice with the CAPS-associa

192 Two compounds caused no detectable skin inflammation in our standard mouse model, documenti

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

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

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

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

197 Allergic skin inflammation in response to epicutaneous (EC) appli

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

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

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

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

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

203 s, which may account for the exacerbation of skin inflammation in some patients who receive anti-TNF

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

205 The hyperproliferative skin inflammation in this novel murine model demonstrate

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

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

208 ack of RabGEF1 results in the development of skin inflammation in vivo.

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

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

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

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

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

214 e role of CCR3 in a murine model of allergic skin inflammation induced by repeated epicutaneous sensi

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

216 f interleukin (IL)-8, a chemokine pivotal to skin inflammation induced by UVB, in epidermal and derma

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

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

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

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

221 of IL-22 in a mouse model where psoriasiform skin inflammation is triggered by topical application of

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

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

224 Skin inflammation measured as Psoriasis Area and Severit

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

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

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

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

229 s 4 and 5 in calcium ionophore-induced acute skin inflammation model demonstrated similar topical pot

230 nce of this inhibition was demonstrated in a skin inflammation model induced by repeated application

231 a T-helper type 2 (Th2)-cell-mediated mouse skin inflammation model that mimics several of the featu

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

233 romoted inflammation in an imiquimod-induced skin-inflammation model, it exerted protective functions

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

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

236 Acute skin inflammation occurs following topical aminolevulini

237 Strikingly, skin inflammation occurs independently of adaptive immun

238 sp., but these microbes usually do not cause skin inflammation or infection in healthy individuals.

239 This decrease in skin inflammation paralleled decreases in splenic neutro

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

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

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

243 Long-term use of topical corticosteroids in skin inflammation poses risks of systemic and local side

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

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

246 The expression of GITRL in skin inflammation remains unknown.

247 Our findings implicate allergic skin inflammation resulting from local Treg deficiency i

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

249 Skin inflammation significantly improved in KC-Tie2 mice

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

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

252 310 SUMOylation site, revealed a more severe skin inflammation than in WT mice.

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

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

255 inflammation was used to define mediators of skin inflammation that may have clinical relevance.

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

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

258 9 was genetically deleted in mouse models of skin inflammation, the psoriasis-like skin disease and i

259 Skin inflammation; thrombosis clotting times; and percen

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

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

262 rally immunized WT mice transferred allergic skin inflammation to naive recipients cutaneously challe

263 in normally, but failed to transfer allergic skin inflammation to WT recipients.

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

265 ike" efficacy in a chronic dust-mite antigen skin inflammation treatment model.

266 -specific T-cell priming and T-cell-mediated skin inflammation, two independent processes essential f

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

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

269 ed a mouse model of TLR7- and TLR9-dependent skin inflammation using tape stripping.

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

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

272 Skin inflammation was assessed by SCORAD.

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

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

275 Skin inflammation was induced in BALB/c scid/scid mice a

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

277 Moreover, skin inflammation was reduced by cotreatment with the TN

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

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

280 n a severe systemic autoimmune reaction with skin inflammation, wasting, and death.

281 of galectin-3 in the development of allergic skin inflammation, we compared inflammatory skin respons

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

283 Using an ovine model of granulomatous skin inflammation, we demonstrate that B cells increase

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

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

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

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

288 genic mice, which develop spontaneous atopic skin inflammation, were found by immunofluoresence, to h

289 tor in the skin to protect MRL/lpr mice from skin inflammation, whereas its inhibitory role in the in

290 ecruited hierarchically to induce neurogenic skin inflammation, which inhibits hair growth.

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

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

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

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

295 ovides a novel mechanism of reducing chronic skin inflammation with improved skin homeostasis and min

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

297 with ovalbumin (OVA), which causes allergic skin inflammation with many characteristics of the skin

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

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

300 cluding elevated serum IgE levels and severe skin inflammation, with infiltrates of both lymphocytes