ライフサイエンスコーパス: imiquimod

1 TLR-4 [lipopolysaccharide (LPS)], and TLR-7 (imiquimod).

2 IL-23 or by application of the TLR7 agonist imiquimod.

3 ion in response to the inflammatory mediator imiquimod.

4 by poly(I.C) of TLR3 but not of TLR7/8 with imiquimod.

5 mly allocated cidofovir and 91 were assigned imiquimod.

6 ike skin symptoms following stimulation with imiquimod.

7 and by 42 (46%; 37.2-55.3) patients assigned imiquimod.

8 psoriasis-like skin inflammation induced by imiquimod.

9 ld enhance chemokine expression initiated by imiquimod.

10 n was topically inflamed by the TLR7 agonist imiquimod.

11 s, as do sensing of viral ssRNA and the drug imiquimod.

12 in patients in response to stimulation with imiquimod.

13 ring mice completely abolished the effect of imiquimod.

14 by topical application of the TLR7/8 agonist imiquimod.

15 llowed by additional topical applications of imiquimod.

16 LR agonists, including the pure TLR7 agonist imiquimod.

17 l antibody blocked the protective effects of imiquimod.

18 ation of the innate immune response modifier imiquimod.

19 deoxynucleotides (ODN), or the TLR7 agonist, imiquimod.

20 flammatory signature after multiple doses of imiquimod.

21 topical toll-like receptor (TLR)-7 agonist, imiquimod.

22 y topical administration of the TLR7 agonist imiquimod.

23 s sense haptens, pDCs are primary sensors of imiquimod.

24 it for lesions that respond early to topical imiquimod.

25 , acitretin (2 trials, 61 participants), and imiquimod (1 trial, 20 participants) compared to control

26 Imiquimod (1-(2-methylpropyl)-1H-imidazo[4,5-c]quinolin-

27 failure was 2.03 (95% CI, 1.36 to 3.04) with imiquimod, 2.73 (95% CI, 1.87 to 3.99) with MAL-PDT, and

28 reported previously led to the discovery of imiquimod, 26, which was developed as a topical agent an

29 A new formulation of imiquimod (3.75% cream) is recommended for AGW treatment

30 Participants were randomized to imiquimod 5% cream once daily (superficial basal cell ca

31 by centre and tumour type, to receive either imiquimod 5% cream once daily for 6 weeks (superficial)

32 Imiquimod 5% cream was effective in the treatment of AK,

33 via administration of the selective agonist imiquimod (5.0 mg/kg) induces a phenotype in offspring c

34 Imiquimod, 5%, and the Mw vaccine were equally effective

35 Patients received either imiquimod, 5%, cream and an intralesional vehicle (imiqu

36 lesional Mw vaccine is comparable to that of imiquimod, 5%, in treatment of AGWs.

37 66.8 to 81.0) than among those who received imiquimod (53.9%; 95% CI, 45.4 to 61.6), MAL-PDT (37.7%;

38 In this report, topical imiquimod, a synthetic TLR7 agonist, significantly enhan

39 Imiquimod, a TLR 7 agonist, has been found to be efficac

40 ns, groups of mice were injected with viral (Imiquimod, a TLR7 agonist) or bacterial (ODN 2395, a TLR

41 luated the safety and feasibility of topical imiquimod, a TLR7 agonist, in a series of vaccinations a

42 Imiquimod-activated chemokine expression was dependent u

43 Continuous imiquimod administration in CNS tumor-bearing mice, howe

44 We additionally demonstrated that imiquimod administration significantly increased the acc

45 a more robust inflammatory response than did imiquimod after inoculation into the CNS, with higher le

46 with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists showed decreased proliferation and a

47 Imiquimod (Aldara 5% cream; 3M Pharmaceuticals, St Paul,

48 atment for the first 4 recipients of topical imiquimod, all of whom displayed a marked improvement of

49 APCs from mice treated with UV irradiation, imiquimod alone or the combination of UV irradiation and

50 were significantly enhanced in poly (I: C), imiquimod along with inactivated PRRSV group.

51 Imiquimod also enhanced DNA repair of UV light (UVL)-irr

52 SCCs treated in vitro with imiquimod also expressed vascular E-selectin.

53 In vivo and in vitro treatment with imiquimod also induced IL-6 production by effector T cel

54 However, both CpG ODN and imiquimod also induced proinflammatory cytokine expressi

55 topically with available anti-cancer drugs (imiquimod and 5-fluorouracil).

56 Th2-biased skin inflammation in response to imiquimod and associated a low level of TRIM32 with AD.

57 Imiquimod and CL097 inhibited the quinone oxidoreductase

58 Recently, a combination therapy of imiquimod and GV has shown an inhibitory effect against

59 del antigen ovalbumin (OVA) and TLR agonists imiquimod and monophosphoryl Lipid A encapsulated in pol

60 In contrast, two other adjuvants, imiquimod and Quil A saponin, favored an expansion of an

61 r TNF-alpha in response to the TLR7 agonists imiquimod and Sendai virus and to the TLR9 agonist CpG.

62 s of 83.6% (178/213) and 98.4% (185/188) for imiquimod and surgery, respectively.

63 rs in only 2 cases, and the immunomodulators imiquimod and thalidomide allowed 5 patients to reach su

64 the mechanism of inflammasome activation by imiquimod and the related molecule CL097 and determined

65 e examined the potential of the TLR7 agonist imiquimod and the TLR9 agonist cytosine-phosphate-guanos

66 alpha following stimulation with TLR7 ligand imiquimod and TLR9 ligand CpG ODN-2216 was also impaired

67 tively isolated CLL cells by using anti-IgM, imiquimod, and CpG oligodeoxynucleotide for BCR, TLR7, a

68 were challenged with Aldara, which contains imiquimod, and is used as an experimental model to induc

69 Potent pDC-activating stimuli, such as CpG, imiquimod, and Sendai virus, induced the most Tim-3 expr

70 These data suggest that topical imiquimod applications may play a role in preventing UV-

71 d ISG15 on stimulation with the TLR7 agonist imiquimod as compared with family members and controls.

72 ity of two topical treatments--cidofovir and imiquimod--as an alternative to surgery in female patien

73 current studies, the topical application of imiquimod at the site of subcutaneously injected Plasmod

74 rstand the immunological mechanisms by which imiquimod augmented antitumor immunity, we tested whethe

75 nt of donor-derived DCs to the skin, whereas imiquimod augmented their alloreactivity.

76 SCC treated with imiquimod before excision contained dense T-cell infiltr

77 d with the Toll-like receptor (TLR)7 agonist imiquimod before excision showed induction of E-selectin

78 t TGF-beta, enhanced the antitumor effect of imiquimod by significantly prolonging survival in treate

79 In conclusion, we have shown that topical imiquimod can induce a robust immune response in breast

80 onstrate that treatment with the TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, resulting in t

81 that topical treatment with a TLR-7 agonist, imiquimod, can elicit significant regression of spontane

82 duction by Vgamma4(+) gammadeltaT cells upon imiquimod challenge.

83 esolve inflammation after discontinuation of imiquimod challenge.

84 d modest clinical 3-year benefit for topical imiquimod compared with surgery for superficial or nodul

85 nce occurred in 50% of patients treated with imiquimod, compared to 5% treated with vehicle, and the

86 however, neonatal TNF-alpha responses to the imiquimod congener R-848 (TLR 7/8) were fully intact.

87 adjunctive treatment with the TLR-7 agonist imiquimod could augment antitumor immune responsiveness

88 In this setting, imiquimod could be utilized in combination with other ta

89 skin inflammation by topical treatment with imiquimod cream (Aldara).

90 treatment for low-risk basal-cell carcinoma, imiquimod cream might still be a useful treatment option

91 tly, topical treatment of mouse skin with 5% imiquimod cream prior to UVL irradiation resulted in a d

92 We aimed to assess the effectiveness of imiquimod cream versus surgical excision in patients wit

93 Treatment of primary melanomas with 5% imiquimod cream was associated with an increase in both

94 Imiquimod cream, 5%, was applied topically to a designat

95 to treatment with 5% fluorouracil cream, 5% imiquimod cream, methyl aminolevulinate photodynamic the

96 primary melanoma biopsy site with placebo or imiquimod cream, we measured immune responses in the tre

97 rmore, CP-456,773 reduces ear swelling in an imiquimod cream-induced mouse model of skin inflammation

98 (polyinosinic-polycytidylic acid) or MyD88 (imiquimod), demonstrating selectivity for C5a regulation

99 nescent, in vivo imaging, we determined that imiquimod dramatically enhanced both the persistence and

100 a simple linear peptide followed by topical imiquimod elicited strong Th1 CD4(+) T-cell responses, a

101 support the idea that TLR7 agonists such as imiquimod enhance DNA repair in bone marrow-derived cell

102 Imiquimod enhanced the expression of xeroderma pigmentos

103 To test our hypothesis that imiquimod enhances DNA repair as a mechanism for its ant

104 in psoriasiform skin significantly reversed imiquimod-established chronic itch and cutaneous inflamm

105 nociceptors, DDCs failed to produce IL-23 in imiquimod-exposed skin.

106 Although topical imiquimod exposures before UV light did not prevent the

107 Upon skin challenge with imiquimod, eYFP(+) gammadelta and CD4 T cells expanded i

108 1 participants were randomly assigned to the imiquimod group (n=254) or the surgical excision group (

109 nalysis, 59% (n = 26) of the patients in the imiquimod group and 67% (n = 30) of those in the Mw grou

110 vents in 99 (40%) of 249 participants in the imiquimod group and 97 (42%) of 229 in the surgery group

111 ents in the cidofovir group and seven in the imiquimod group either withdrew or were lost to follow-u

112 rse events were itching (211 patients in the imiquimod group vs 129 in the surgery group) and weeping

113 years, 178 (84%) of 213 participants in the imiquimod group were treated successfully compared with

114 12 (5%) participants in the imiquimod group withdrew because of adverse events compa

115 4 x 108 copies/mg of tissue; P = .01) in the imiquimod group.

116 mod, 5%, cream and an intralesional vehicle (imiquimod group: 44 patients) or vehicle cream and intra

117 Recently, imiquimod has demonstrated tumor regression in melanoma

118 TLR7 activation by imiquimod has pleiotropic effects on innate immune cells

119 Imiquimod has TLR7-independent activities that are mecha

120 Indeed, synthetic TLR agonists such as imiquimod have already established utility in treating v

121 ments, only photodynamic therapy and topical imiquimod have become established treatments for specifi

122 and improvement in warts in combination with imiquimod; however, immunoglobulin levels and specific v

123 small-molecule toll-like receptor 7 agonist, imiquimod (IMD), and a hydrophilic macromolecule, anti-C

124 duced models of skin inflammation induced by imiquimod (IMQ) and IL-23 and tested the effect of inhib

125 l carcinoma (PNBCC) following treatment with imiquimod (IMQ) has not yet been established.

126 aining the Toll-like receptor (TLR)7 agonist Imiquimod (IMQ) onto patients induces flares of psoriasi

127 Following exposure to the inflammatory agent imiquimod (IMQ) the Vgamma4(+) subset of gammadeltaT cel

128 with the Toll-like receptor 7 (TLR7) agonist imiquimod (IMQ) to activate IFN-sensitive gene (ISG) pat

129 d that short-term, 5-7 d-long application of imiquimod (IMQ), a TLR7 agonist, to the skin of mice tri

130 Despite its useful properties, imiquimod (IMQ), known as an anti-cancer drug, can be ha

131 e model of psoriasis induced by TLR7 agonist imiquimod (IMQ), we show that VISTA deficiency exacerbat

132 Similarly, the imiquimod (IMQ)- and Il23-induced mouse psoriasis was as

133 Similarly, MCPIP1 was overexpressed in the imiquimod (IMQ)-driven mouse model of cutaneous inflamma

134 he initiation phase of autophagy, attenuates imiquimod (IMQ)-induced epidermal hyperplasia in adult m

135 -1KO) mice and wild-type (WT) controls in an imiquimod (IMQ)-induced murine model of psoriasis.

136 lysaccharide (LPS)-induced keratinocytes and imiquimod (IMQ)-induced psoriasiform dermatitis in mice.

137 elta or PI3Kgamma are largely protected from imiquimod (IMQ)-induced psoriasis-like dermatitis, corre

138 her macrophages are activated in the skin of imiquimod (IMQ)-treated mice, a model for IL-17A-induced

139 At a functional level, both TLR7/8- (imiquimod [IMQ]) and TLR9-stimulated (CpG2216) pDCs lyse

140 ent tumor samples from patients treated with imiquimod in a clinical trial were profiled using Nanost

141 ain samples identified significant levels of Imiquimod in both compartments at molar concentrations l

142 ever, the molecular perturbations induced by imiquimod in breast cancer metastases have not been prev

143 c profiles associated with responsiveness to imiquimod in breast cancer skin metastases.

144 safety and objective response rate (ORR) of imiquimod in combination with systemic albumin bound pac

145 al, and systemic immune responses induced by imiquimod in patients with high-risk melanoma.

146 L-12 was important in the protective role of imiquimod in preventing UV-induced loss of CHS, as syste

147 ther evidence for a TLR7-independent role of imiquimod in the epithelial immune response and reinforc

148 Topical application of imiquimod in vivo led to epidermal microabscess formatio

149 kin lesions induced by daily applications of imiquimod in wild-type mice were almost totally absent i

150 Particular local adverse events with imiquimod included erythema (27%), scabbing or crusting

151 ma symptoms induced by daily applications of imiquimod increased dramatically in human IL-26 transgen

152 one or the combination of UV irradiation and imiquimod indicated the same in vivo synergy between imi

153 Treatment of normal human skin with imiquimod induced activation of resident T cells and red

154 The TLR7 agonist imiquimod induced astrocyte activation and up-regulation

155 Inhibition of imiquimod induced cytokine production required residues

156 Compared with untreated skin, topical imiquimod induced dermal mononuclear cell infiltrates in

157 is using tumor-derived RNA demonstrated that imiquimod induced high levels of IL-10 in addition to TN

158 stigated the role of icIL-1Ra1 in Aldara (5% imiquimod)-induced psoriasis-like skin inflammation.

159 elta T cells and CD8(+) Tc17 cells; 2) block imiquimod-induced cutaneous inflammation; 3) inhibit Th1

160 ibited significantly reduced inflammation in imiquimod-induced dermatitis, and were resistant to indu

161 asis-like skin lesions in mice, and improved imiquimod-induced disruption of skin barrier.

162 eficient (Il36r-/-) mice were protected from imiquimod-induced expansion of dermal IL-17-producing ga

163 d was associated with reduced rhinovirus and imiquimod-induced IFN responses by these cells compared

164 muli, and that CP-456,773 inhibits R848- and imiquimod-induced IL-1beta release.

165 lutely required for IL-22 production because imiquimod-induced IL-22 expression in the skin is still

166 phenotype, as well as the transcriptome, of imiquimod-induced inflammation in human skin resembles a

167 stemic treatment with ustekinumab diminished imiquimod-induced inflammation.

168 Using an imiquimod-induced model of immune-mediated epidermal hyp

169 cultures, in vitro migration assays, and the imiquimod-induced model of psoriasiform skin inflammatio

170 using S100a8(-/-) and S100a9(-/-) mice in an imiquimod-induced model of psoriasis.

171 ICZ reduced the inflammatory response in the imiquimod-induced model of skin inflammation and AhR-def

172 g miR-146a(-/-) mice in conjunction with the imiquimod-induced mouse model of psoriasis.

173 t amplifying cells in human psoriasis and in imiquimod-induced murine psoriasis.

174 nd inflammatory dendritic cells, whereas the imiquimod-induced population comprised gammadelta T cell

175 Imiquimod-induced psoriasiform dermatitis was exacerbate

176 t-induced steatohepatitis on the severity of imiquimod-induced psoriasiform dermatitis.

177 The severity of imiquimod-induced psoriasiform inflammation was greatly

178 sively demonstrated using the mouse model of imiquimod-induced psoriasiform skin lesions.

179 s macrophage polarization and contributes to imiquimod-induced psoriasis by sustaining inflammation,

180 on and in skin inflammation using a model of imiquimod-induced psoriasis in mice.

181 In an imiquimod-induced psoriasis model, the administration of

182 at in mice via TMP778 administration reduced imiquimod-induced psoriasis-like cutaneous inflammation.

183 e primary keratinocyte cell cultures and the imiquimod-induced psoriasis-like mouse model of skin inf

184 We investigated the role of IL-26 in the imiquimod-induced psoriasis-like murine model using huma

185 ing genetically modified mice, we found that imiquimod-induced psoriasis-like skin inflammation was c

186 vealed that chrysin significantly attenuated imiquimod-induced psoriasis-like skin lesions in mice, a

187 Using an imiquimod-induced psoriasis-like skin model, we show tha

188 cal roles of CIKS/Act1-mediated signaling in imiquimod-induced psoriatic inflammation, a mouse model

189 f PCSK9 in lesions of psoriasis patients and imiquimod-induced psoriatic reactions in Pcsk9-knockout

190 ling IL-22 during skin inflammation, we used imiquimod-induced skin disease in rodents and showed tha

191 In contrast, tapinarof has no impact on imiquimod-induced skin inflammation in AhR-deficient mic

192 t source of IL-17 in acute murine IL-23- and imiquimod-induced skin inflammation, in human psoriasis

193 Whereas IL-17C promoted inflammation in an imiquimod-induced skin-inflammation model, it exerted pr

194 We demonstrate that imiquimod induces a monomorphic and self-limited inflamm

195 In human subjects imiquimod induces contact dermatitis with the distinctiv

196 Treatment of T reg cells in vitro with imiquimod inhibited their suppressive activity and reduc

197 Imiquimod (IQ) is an agonist of Toll-like receptor 7 (TL

198 d indicated the same in vivo synergy between imiquimod irradiation and UV irradiation in enhancing IL

199 Imiquimod is a cream-formulated, TLR7 agonist that is Fo

200 Imiquimod is a small-molecule ligand of Toll-like recept

201 Imiquimod is a synthetic compound with antitumor propert

202 Imiquimod is a synthetic Toll-like receptor 7 (TLR7) ago

203 Imiquimod is a TLR agonist that is used as an antitumor

204 Imiquimod is a TLR7/8 agonist that has anticancer therap

205 Imiquimod is a topical immune response modifier and Toll

206 Imiquimod is a topical toll-like-receptor-7 agonist curr

207 The antitumor effect of imiquimod is multifactorial, although its ability to mod

208 eptor 7/8 by means of topical application of imiquimod is the most commonly used mouse model of psori

209 ontaining the Toll-like receptor 7/8 agonist Imiquimod, is a widely used mouse model for investigatin

210 Imiquimod leads to an 80-100% cure rate of lentigo malig

211 our hypothesis that topical applications of imiquimod may protect the skin immune system against the

212 ex I inhibition and endolysosomal effects of imiquimod might also contribute to NLRP3 activation.

213 ired for psoriasis-like lesions in the mouse imiquimod model and is produced by both T cells and inna

214 Despite these shortcomings, the human imiquimod model might be useful to investigate early pat

215 Nevertheless, the imiquimod model mimics the hallmarks of psoriasis.

216 ing innate-like T cell populations in a TLR7 imiquimod model of psoriasis-like disorder, indicating t

217 The imiquimod model requires careful consideration and warra

218 3-induced ear swelling model and the topical imiquimod model, and significantly reduced the number of

219 tion and thickness in both the Rac1(V12) and imiquimod mouse models of psoriasis.

220 the systemic immune response induced by the imiquimod/NY-ESO-1 combination, and show that it elicite

221 treated with poly (I: C) of TLR3 ligand and imiquimod of TLR7 ligand, along with inactivated PRRSV a

222 a gel in a 10 g tube, to last 6 weeks) or 5% imiquimod (one 250 mg sachet for every application), to

223 n C57BL/6 mice (PASI score of 1) compared to imiquimod-only treatment (PASI score of 4).

224 parable to Tacrolimus but markedly less than imiquimod-only treatment.

225 se, and secreted cytokines after exposure to imiquimod or lipopolysaccharide.

226 ics develop exacerbated psoriasis induced by imiquimod or recombinant IL-23 injection when challenged

227 a Toll-like receptor 4 (TLR4) (EM005), TLR7 (imiquimod), or TLR9 (CpG DNA) agonist during immunizatio

228 Since 2009, the imiquimod- or Aldara-induced (3M Pharmaceuticals, St. Pa

229 o harm for one additional adverse event with imiquimod over 12-16 weeks ranged from 3.2 to 5.9.

230 ught to investigate the potential of a human imiquimod patch test model to resemble human psoriasis.

231 re cancer-specific interventions (acitretin, imiquimod, photodynamic therapy, nicotinamide, topical d

232 The results suggest that imiquimod positively influences DC trafficking and the p

233 protein was administered intradermally into imiquimod preconditioned sites followed by additional to

234 CpG oligonucleotides and imiquimod, prototypic drugs in this category, are now kn

235 soriatic lesions and both the c-Jun/JunB and imiquimod psoriasis mouse model allowed us to study the

236 The TLR7 agonist imiquimod (R837) caused rapid dose-dependent relaxation

237 ially blocked the TLR-7-activating effect of imiquimod (R837), while transfection with the NS4B gene

238 uced by topical phorbol myristate acetate or imiquimod, reduced the inflammation from erythema doses

239 Treatment of mice with 5% imiquimod resulted in synergistic reduction in CNS tumor

240 al compounds such as melatonin, chloroquine, imiquimod, resveratrol, piceatannol, quercetin, and othe

241 Imiquimod's adjuvant effects require further evaluation

242 Skin biopsies were assessed for imiquimod's in situ immunomodulatory effects.

243 els induced by squaric acid dibutylester and imiquimod showed that extracellular signal-regulated kin

244 In vitro imiquimod stimulated production of IL-1alpha and neutrop

245 TLR7 was essential for imiquimod-stimulated pDCs to produce IFN-alpha/beta, whi

246 Thus, imiquimod stimulates tumor destruction by recruiting cut

247 mmation induced by the TLR7 receptor agonist imiquimod subtly yet reproducibly decreases time to skin

248 7.7% (173/177) for surgery (relative risk of imiquimod success = 0.84, 95% confidence interval = 0.77

249 gues demonstrate that topical application of imiquimod suppresses cutaneous melanoma by TLR7-dependen

250 adverse event was substantially higher with imiquimod than with vehicle, and numbers needed to harm

251 for NLRP3 activation and identify targets of imiquimod that might be clinically relevant.

252 dofovir and 39 (46%) of 84 patients assigned imiquimod; the most frequent grade 3 and 4 events were p

253 -mediated effects, we studied the effects of imiquimod therapy on effector T cells infiltrating human

254 However, tumor growth progressed once imiquimod therapy was ended.

255 Although surgery is clearly superior to imiquimod, this study shows sustained benefit for lesion

256 iquimod, TLR7, and as such are stimulated by imiquimod through a novel pathway.

257 HPV16 virus-like particles and treated with imiquimod (TLR7 agonist).

258 tes do not express the putative receptor for imiquimod, TLR7, and as such are stimulated by imiquimod

259 grew poorly in bovine cells pretreated with imiquimod to stimulate interferon production.

260 sted the efficacy of topical applications of imiquimod to treat patients afflicted with this chronic

261 TLR7 ligand imiquimod treated IFN-gamma reporter mice show that CD4(

262 nscriptomic analysis of splenic tissues from imiquimod-treated autoimmune-prone B6.Sle1b mice suffici

263 deltaT17 cells homed normally to the skin of imiquimod-treated CCR6(-/-) mice.

264 ificantly upregulated in the skin lesions of imiquimod-treated human IL-26 transgenic mice and psoria

265 Additionally, only imiquimod-treated mice were resistant to hapten-specific

266 he major source of IL-22 in lymph nodes from imiquimod-treated mice.

267 lating IL-10 were also detected in sera from imiquimod-treated mice.

268 In the vaginal mucosa of imiquimod-treated monkeys, we documented a massive monon

269 ntly elevated in psoriatic lesional skin and imiquimod-treated mouse skin.

270 -1alpha signaling in the microenvironment of imiquimod-treated Ovol1-deficient skin that functionally

271 ly, histologically, and transcriptionally in imiquimod-treated psoriasis-like mouse skin.

272 -selectin expression at levels comparable to imiquimod-treated SCCs undergoing immunologic destructio

273 vo and the mechanism of their recruitment to imiquimod-treated sites have never been demonstrated.

274 gammadeltaT17 cells were greatly reduced in imiquimod-treated skin of CCR6(-/-) mice, but adoptively

275 ifferent composition than those infiltrating imiquimod-treated skin.

276 Imiquimod-treated tumors contained a decreased percentag

277 igorous IFN-gamma production than did either imiquimod-treated XS52 or UV-irradiated XS52, again sugg

278 Imiquimod-treated, UV-irradiated XS52 triggered a more v

279 ecrease the inflammatory reaction induced by imiquimod treatment and inhibit hyperproliferation of ke

280 ocedure, and 16 were offered radiotherapy or imiquimod treatment as a consequence of the RCM findings

281 mented antitumor immunity, we tested whether imiquimod treatment enhanced DC function or the priming

282 Most imiquimod treatment failures occurred in year 1.

283 Our results demonstrate that imiquimod treatment leads to CCL2-dependent recruitment

284 Topical imiquimod treatment led to TLR7-dependent and IFN-alpha/

285 s small pilot study demonstrate that topical imiquimod treatment results in enhanced local and region

286 Additionally, the combination of imiquimod treatment with prior vaccination led to develo

287 major role in neutrophil infiltration after imiquimod treatment.

288 regulatory cells, which were also induced by imiquimod treatment.

289 In responding patients, Imiquimod triggered a strong T-helper-1 (Th-1)/cytotoxic

290 rable contact hypersensitivity reactions and imiquimod-triggered psoriatic skin inflammation, indicat

291 tosis (AK) with the immune response modifier imiquimod was assessed using published randomized-contro

292 Imiquimod was inferior to surgery according to our prede

293 Five-year success rates for imiquimod were 82.5% (170/206) compared with 97.7% (173/

294 Cidofovir and imiquimod were active, safe, and feasible for treatment

295 We exposed the skin of mice to imiquimod, which induces IL-23-dependent psoriasis-like

296 iatic itch after the repeated application of imiquimod, which is a preclinical model of psoriasis.

297 A synthetic TLR7 agonist, imiquimod, which is FDA approved for topical treatment o

298 after topical application of the TLR7 ligand imiquimod, which is known to enhance the LC emigration f

299 Indeed, the association of Imiquimod with the brain correlated with increased Iba1

300 eliorated psoriasiform dermatitis induced by imiquimod, with decreased pro-inflammatory IL-17- and IL