ライフサイエンスコーパス: contact hypersensitivity

1 use of the lack of murine models for chronic contact hypersensitivity.

2 d innate immunity during the early stages of contact hypersensitivity.

3 essed the role of CCR6 on the development of contact hypersensitivity.

4 of 2,4-dinitro-fluorobenzene (DNFB)-induced contact hypersensitivity.

5 C migration to lymph node with the defect in contact hypersensitivity.

6 inflammation: endotoxic shock, diabetes, and contact hypersensitivity.

7 ial asthma, allergic rhinitis, and cutaneous contact hypersensitivity.

8 a distant site also suppressed induction of contact hypersensitivity.

9 regulate keratinocyte function and death in contact hypersensitivity.

10 /)- mice, thereby restoring the capacity for contact hypersensitivity.

11 pathophysiology of the elicitation phase of contact hypersensitivity.

12 IL-17 in an IL-1beta-dependent manner during contact hypersensitivity.

13 might be a potential target for treatment of contact hypersensitivity.

14 00-fold higher dose was required to suppress contact hypersensitivity.

15 odies was able to reverse this impairment of contact hypersensitivity.

16 in the pathogenesis of allergic and irritant contact hypersensitivity.

17 ed with impaired LC function with respect to contact hypersensitivity.

18 cells has an important role in induction of contact hypersensitivity.

19 tenuated ear-swelling response in a model of contact hypersensitivity.

20 fic CD8(+) Treg cells, which protect against contact hypersensitivity.

21 ed protective effects in models of sepsis or contact hypersensitivity.

22 draining lymph nodes following induction of contact hypersensitivity.

23 utaneous application of ovalbumin and during contact hypersensitivity.

24 es to generation of immunity in DNFB-induced contact hypersensitivity.

25 suppression of both CD8 T cell expansion and contact hypersensitivity.

26 onse [delayed-type hypersensitivity (DTH) or contact hypersensitivity].

27 It was efficacious in mouse models of contact hypersensitivity (1 mg/kg b.i.d.) and house dust

28 t LNs are absolutely required for generating contact hypersensitivity, a T cell-dependent cellular im

29 hanced excitability after the development of contact hypersensitivity, an animal model of allergic co

30 ts mimicked by pTpT to include inhibition of contact hypersensitivity and activation of the tumor nec

31 ition, IFN-gammaR2 -/- mice are defective in contact hypersensitivity and are highly susceptible to i

32 to UV exhibit a profound suppression of both contact hypersensitivity and delayed type hypersensitivi

33 Because the regulation of contact hypersensitivity and DTH responses differ, we in

34 t suppressed the CD8 T cell response to both contact hypersensitivity and epicutaneous protein immuni

35 ance was assessed by means of suppression of contact hypersensitivity and hapten-specific IFN-gamma-p

36 mice exhibited a T cell intrinsic defect in contact hypersensitivity and impaired responses to cutan

37 mparable to UVR, suppresses the induction of contact hypersensitivity and induces Ag-specific regulat

38 analyses, we used fluorescein isothiocyanate contact hypersensitivity and ovalbumin-induced dermatiti

39 emonstrate an essential role for IL-1beta in contact hypersensitivity and suggest that IL-1beta acts

40 may not be responsible for the generation of contact hypersensitivity and that dermal dendritic cells

41 ch- and pain-related behaviours accompanying contact hypersensitivity and/or other inflammatory disea

42 ediates ultraviolet-B-induced suppression of contact hypersensitivity, and because pTpT exerts many u

43 induced skin cancers, suppresses delayed and contact hypersensitivity, and depress the ability of den

44 enting cell events in the induction of human contact hypersensitivity, and on the other hand to simul

45 rget for ultraviolet-B-induced inhibition of contact hypersensitivity, and small DNA fragments such a

46 e psoriasis, atopic dermatitis, and allergic contact hypersensitivity are associated with T helper ty

47 Using murine allergic contact hypersensitivity as a model, we investigated the

48 The impairment of contact hypersensitivity, as it develops early and corre

49 Contact hypersensitivity assay (CHS) faithfully models h

50 sed significantly the sensitization phase of contact hypersensitivity assays while inducing a drastic

51 acute conditions, including septic shock and contact hypersensitivity autoimmune diseases, such as rh

52 In contrast, the spleen cannot mediate contact hypersensitivity because antigen-bearing epiderm

53 oil) in a stringent swine model of allergic contact hypersensitivity, but its potency was markedly r

54 Suppression of contact hypersensitivity by local, low-dose UV radiation

55 ic T cell-mediated immune responses, such as contact hypersensitivity (CH) and delayed-type hypersens

56 t B (UVB) radiation impairs the induction of contact hypersensitivity (CH) and induces tolerance in U

57 B7RP-1-Fc stimulated contact hypersensitivity (CH) given near either the time

58 on, we determined whether SP participates in contact hypersensitivity (CH) induction by using a SP ag

59 w-dose ultraviolet B radiation (UVR) impairs contact hypersensitivity (CH) induction in genetically d

60 cell-related skin disease models, including contact hypersensitivity (CHS) and experimental graft-ve

61 es antitumor immunity but also inhibits skin contact hypersensitivity (CHS) and prolongs skin graft s

62 olia, on UVB-induced immunosuppression using contact hypersensitivity (CHS) as a model in C3H/HeN mic

63 strated that, in male rats, the magnitude of contact hypersensitivity (CHS) can be enhanced by morphi

64 d immune responses to dermal vaccination and contact hypersensitivity (CHS) challenge in K14-VEGFR-3-

65 also recruited to inflamed skin in allergic contact hypersensitivity (CHS) contingent on E- and P-se

66 et B (UVB) radiation) and UVB suppression of contact hypersensitivity (CHS) in both the local and the

67 l killer (NK) cells mediate antigen-specific contact hypersensitivity (CHS) in mice deficient in T ce

68 e immune response, we studied its effects on contact hypersensitivity (CHS) in response to two allerg

69 Hapten-induced contact hypersensitivity (CHS) in the skin is a delayed

70 Contact hypersensitivity (CHS) is a CD8 T cell-mediated

71 Contact hypersensitivity (CHS) is a CD8+ T cell-mediated

72 Contact hypersensitivity (CHS) is a T cell response to h

73 Allergen-induced contact hypersensitivity (CHS) is a T cell-mediated dela

74 Contact hypersensitivity (CHS) is a T cell-mediated resp

75 Contact hypersensitivity (CHS) is a T cell-mediated resp

76 he DC status of CD40 ligand -/- mice using a contact hypersensitivity (CHS) model system that enables

77 e, Lehtimaki et al. use an oxazolone-induced contact hypersensitivity (CHS) model to show that T cell

78 have been intensively investigated by using contact hypersensitivity (CHS) models in mice.

79 Contact hypersensitivity (CHS) of murine skin serves as

80 icular dendritic cells and failed to develop contact hypersensitivity (CHS) or form germinal centers

81 BH) protocol to BALB/c mice experiencing the contact hypersensitivity (CHS) reaction.

82 itical for the initiation and propagation of contact hypersensitivity (CHS) reactions have yielded co

83 ation to inflamed skin, we elicited allergic contact hypersensitivity (CHS) reactions in mice treated

84 atopic dermatitis, and is known to suppress contact hypersensitivity (CHS) reactions in mouse models

85 It is caused by CD8(+) T cell-mediated contact hypersensitivity (CHS) reactions triggered at th

86 R agonists and PAF-R-dependent inhibition of contact hypersensitivity (CHS) reactions, indicating a r

87 r define the mechanism by which UVB inhibits contact hypersensitivity (CHS) reactions.

88 Contact hypersensitivity (CHS) requires activation of th

89 e model for allergic contact dermatitis, the contact hypersensitivity (CHS) response to the obligate

90 strointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previou

91 overexpression in keratinocytes on a classic contact hypersensitivity (CHS) response.

92 g L-selectin-deficient mice, that defects in contact hypersensitivity (CHS) responses are in essence

93 ate immune components that modulate allergic contact hypersensitivity (CHS) responses are poorly defi

94 ure to noonday summer sunlight, can suppress contact hypersensitivity (CHS) responses in healthy whit

95 arization by ribavirin in vivo could promote contact hypersensitivity (CHS) responses to dinitrofluor

96 The primary effector cells of contact hypersensitivity (CHS) responses to dintrofluoro

97 aviolet B radiation impairs the induction of contact hypersensitivity (CHS) responses to haptens appl

98 phenotype which includes strikingly impaired contact hypersensitivity (CHS) responses to reactive hap

99 sensitization with dinitrofluorobenzene for contact hypersensitivity (CHS) responses, hapten-specifi

100 in opposite conclusions about their role in contact hypersensitivity (CHS) responses.

101 stitutively lack LCs and develop exaggerated contact hypersensitivity (CHS) responses.

102 CIP4(-/-) mice also had impaired contact hypersensitivity (CHS) to haptens, and their T c

103 10-deficient (IL-10(-/-)) mice have enhanced contact hypersensitivity (CHS) to topical hapten.

104 Unexpectedly, we found that contact hypersensitivity (CHS) was amplified rather than

105 contribute to the adaptive immune response, contact hypersensitivity (CHS) was characterized in mice

106 -12 play a pivotal role in the initiation of contact hypersensitivity (CHS), a Th1 immune response in

107 dels of delayed-type hypersensitivity (DTH), contact hypersensitivity (CHS), and arthritis.

108 gic contact dermatitis and its animal model, contact hypersensitivity (CHS), are T cell-mediated infl

109 skin to hapten sensitization and challenge, contact hypersensitivity (CHS), is negatively regulated

110 independent T cell-mediated immune response, contact hypersensitivity (CHS), was used to further inve

111 sed a model of T cell-mediated inflammation, contact hypersensitivity (CHS), where priming of the eff

112 growth factors, during wound healing and in contact hypersensitivity (CHS)--induced inflammation whe

113 gulated during inflammation induced by acute contact hypersensitivity (CHS).

114 ne (DNTB), differ in their ability to induce contact hypersensitivity (CHS).

115 in vitro, and are thought to be involved in contact hypersensitivity (CHS).

116 rated to be a critical effector molecule for contact hypersensitivity (CHS).

117 ibute to the expression of certain models of contact hypersensitivity (CHS).

118 dinitrofluorobenzene (DNFB)-induced model of contact hypersensitivity (CHS).

119 ll-mediated inflammatory skin disease called contact hypersensitivity (CHS).

120 -mediated immunity (CMI) reflected by nickel contact hypersensitivity (CHS).

121 nction and the established MC-driven disease contact hypersensitivity (CHS).

122 c disease, allergic airway inflammation, and contact hypersensitivity (CHS).

123 al Langerhans cells (LC) develop exaggerated contact-hypersensitivity (CHS) responses due to the abse

124 In contact hypersensitivity, collagen-induced arthritis, an

125 an inability to induce normal cell-mediated contact hypersensitivity, despite the ability of the cel

126 ronic inflammation, we examined delayed-type contact hypersensitivity (DTH) responses in P-selectin,

127 elicitation (but not sensitization) phase of contact hypersensitivity exacerbated ear-swelling respon

128 l models of acute dermatitis, mixed allergic contact hypersensitivity, focal arthritis and spontaneou

129 ed by mast cells could mediate impairment of contact hypersensitivity in a manner similar to that fou

130 CS exposure inhibits contact hypersensitivity in a PAF-R-dependent manner as

131 rmatitis (ACD) using an established model of contact hypersensitivity in C57Bl/6 mice utilizing 2,4-d

132 Contact hypersensitivity in Langerin-Cre MyD88(fl) mice

133 ene-related peptide impairs the induction of contact hypersensitivity in mice, and participates in th

134 lly, GADD45gamma deficiencies caused reduced contact hypersensitivity in mice.

135 emonstrate a role for TSLP in a Th2 model of contact hypersensitivity in mice.

136 determining the induction and elicitation of contact hypersensitivity in PKR:(-/-) mice, a model of T

137 as to the inflammation observed at sites of contact hypersensitivity in response to oxazolone.

138 of delayed-type hypersensitivity in mice and contact hypersensitivity in rodents and humans.

139 elongation of cutaneous nerve fibers during contact hypersensitivity in the mouse.

140 undly inhibited dinitrochlorobenzene-induced contact hypersensitivity in the pig by 78% and 90%, resp

141 sequent challenge revealed a 60% decrease in contact hypersensitivity in TPA-treated mice.

142 injection of hapten-conjugated XS-DC induced contact hypersensitivity in vivo, suggesting their poten

143 s similar to the effector cells that mediate contact hypersensitivity in vivo.

144 tokine gene expression during elicitation of contact hypersensitivity in which expression of IP-10 is

145 e-specific inhibitor SU11274 also suppressed contact hypersensitivity in wild-type mice.

146 In contrast, severity of hapten-induced contact hypersensitivity, in which CD8 T cells and NK ce

147 milar requirement in an established model of contact hypersensitivity, in which IDO2-expressing B cel

148 ric acid dibutyl ester, produced symptoms of contact hypersensitivity including an increase in skin t

149 ogical memory in the form of hapten-specific contact hypersensitivity independent of T and B cells.

150 -cell-mediated skin inflammation by assaying contact hypersensitivity indicated an increased response

151 In the contact hypersensitivity induced by oxazolone, the OGG-1

152 is required for the development of Th2-type contact hypersensitivity induced by the hapten FITC in c

153 SAA1 expression was also demonstrated during contact hypersensitivity induced by topical application

154 d participates in the pathogenesis of failed contact hypersensitivity induction after acute, low-dose

155 strated that ultraviolet B radiation impairs contact hypersensitivity induction in ultraviolet B susc

156 As ultraviolet B radiation impairs contact hypersensitivity induction through a tumor necro

157 Contact hypersensitivity induction was impaired in ultra

158 that ultraviolet B radiation did not impair contact hypersensitivity induction when haptens were pai

159 n of the hapten-specific signal required for contact hypersensitivity induction.

160 ment of both acute (croton oil) and chronic (contact hypersensitivity) inflammation at sites of the s

161 Contact hypersensitivity is a CD8 T cell-mediated respon

162 ltraviolet B radiation induced impairment of contact hypersensitivity is not uniform in all individua

163 Based on murine studies of acute contact hypersensitivity, mast cells (MCs) are believed

164 , and keratinocyte proliferation in a murine contact hypersensitivity model and inhibited tissue infl

165 We developed and used a chronic contact hypersensitivity model in wild-type and MC-defic

166 A contact hypersensitivity model using IL-9(-/-) mice show

167 In a contact hypersensitivity model, the infiltration of CD4(

168 In the contact hypersensitivity model, this was associated with

169 In the dinitrofluorobenzene contact hypersensitivity model, UV-irradiated MyD88-defi

170 Unlike the contact hypersensitivity model, which is induced by pote

171 migration into the inflamed skin in a murine contact hypersensitivity model.

172 he epidermis of mice in an oxazolone-induced contact hypersensitivity model.

173 orescein isothiocyanate (FITC) and oxazolone contact hypersensitivity models, WASp-null Langerhans ce

174 During contact hypersensitivity, murine P-selectin messenger (m

175 idermal immune function use the induction of contact hypersensitivity or epidermal cell alloantigen p

176 bserved for systemic UV immunosuppression of contact hypersensitivity (p < 0.025).

177 ivity response to hapten by using a modified contact hypersensitivity protocol.

178 Although murine contact hypersensitivity provides a framework for unders

179 oimmune encephalomyelitis, and had defective contact hypersensitivity reaction and local Ag-induced r

180 umor necrosis factor-alpha and in vivo via a contact hypersensitivity reaction or herpes simplex viru

181 Contact hypersensitivity reactions in response to variou

182 y deficient mice, moreover, developed weaker contact hypersensitivity reactions to haptens applied ep

183 We found that contact hypersensitivity reactions to oxazolone in mice

184 was unimpaired in homozygous mutant animals, contact hypersensitivity reactions were compromised.

185 nted up-regulation of P-selectin mRNA during contact hypersensitivity reduced P-selectin-dependent in

186 /-) mice were impaired in the development of contact hypersensitivity relative to gal3(+/+) mice in r

187 mmune compartment, demonstrated an increased contact hypersensitivity response and decreased control

188 reduction in the 1-fluoro-2,4-dinitrobenzene contact hypersensitivity response and resulted in the in

189 The SPARC-null mice also exhibited a limited contact hypersensitivity response and were refractory to

190 Additionally, the contact hypersensitivity response generated in wild-type

191 ared normal as assessed by evaluation of the contact hypersensitivity response in cpdm/cpdm mice.

192 resistant P2 agonist, results in an enhanced contact hypersensitivity response in mice.

193 Inhibition of contact hypersensitivity response in the sICAM-1 transge

194 of cDC following TBI results in an impaired contact hypersensitivity response to hapten by using a m

195 Allergic contact hypersensitivity response to oxazolone and oxazo

196 -deficient mice also demonstrate an impaired contact hypersensitivity response to the hapten trinitro

197 Contact hypersensitivity response was evaluated by measu

198 The contact hypersensitivity response was significantly supp

199 for sunburn/erythema and suppression of the contact hypersensitivity response were generated either

200 Mice lacking Ox40L exhibit an impaired contact hypersensitivity response, a dendritic cell-depe

201 ition, IP-10(-/-) mice exhibited an impaired contact hypersensitivity response, characterized by decr

202 During the elicitation of the contact hypersensitivity response, endothelial cells exp

203 th previous data, we here report a decreased contact hypersensitivity response, induced by 2,4,-dinit

204 out (CD4(-/-)) mice developed an exaggerated contact hypersensitivity response.

205 evelopment of LZT, resulting in a pronounced contact hypersensitivity response.

206 rment in lymphocyte homing and a compromised contact hypersensitivity response.

207 .A(R1) mice, which are Kk and Id, a vigorous contact-hypersensitivity response was present, indicatin

208 Contact hypersensitivity responses (CHS) to dinitrochlor

209 Orai1(KI/KI) mice lacked detectable contact hypersensitivity responses and tolerated skin al

210 n of EpCAM-deficient LC resulted in enhanced contact hypersensitivity responses as previously describ

211 nduction during DNFB sensitization increased contact hypersensitivity responses by 1.5-fold.

212 athways of delayed-type hypersensitivity and contact hypersensitivity responses by UVR differ.

213 HSP27 had an increased capacity to initiate contact hypersensitivity responses compared with control

214 Allergic contact hypersensitivity responses in BALB/c mice to oxa

215 s.c. administration of GR1 impaired in vivo contact hypersensitivity responses in mice and was assoc

216 tration of Pep-1 inhibited the expression of contact hypersensitivity responses in mice by blocking s

217 en compared with wild type, the magnitude of contact hypersensitivity responses in PKR:(-/-) mice wer

218 ogeneic stimulation in vitro and exacerbated contact hypersensitivity responses in vivo.

219 Ear swelling chronic contact hypersensitivity responses increased markedly, u

220 urine skin in vivo impaired the induction of contact hypersensitivity responses initiated either loca

221 ndritic cells nor the increased induction of contact hypersensitivity responses occurred in TLR4-defi

222 Depletion of CD4+ T cells resulted in contact hypersensitivity responses of higher magnitude a

223 Consequently, these mice had lower contact hypersensitivity responses than those of wild-ty

224 hapten challenge led to markedly suppressed contact hypersensitivity responses that lasted 3 wk and

225 T cells and B cells demonstrated substantial contact hypersensitivity responses to 2,4-dinitrofluorob

226 n BALB/c mice to oxazolone, but not irritant contact hypersensitivity responses to croton oil, were s

227 sensitivity responses to C. albicans but not contact hypersensitivity responses to dinitrofluorobenze

228 bility of Aloe gel to prevent suppression of contact hypersensitivity responses to hapten decayed rap

229 dependent antigen-specific receptors mediate contact hypersensitivity responses to haptens.

230 st, IL-1beta-deficient mice showed defective contact hypersensitivity responses to topically applied

231 Contact hypersensitivity responses were acquired by such

232 Sixteen weeks after reconstitution, contact hypersensitivity responses were significantly re

233 sensitized to that antigen, then subsequent contact hypersensitivity responses were significantly re

234 red for efficient priming of hapten-specific contact hypersensitivity responses, but was dispensable

235 bore the same TCR, TRM cells mediated rapid contact hypersensitivity responses, whereas TCM cells me

236 erance induction to hapten sensitization and contact hypersensitivity responses.

237 ans cell migration results in suppression of contact hypersensitivity responses.

238 e in the skin led to impaired hapten-induced contact hypersensitivity responses.

239 e, Bcl-3 in endogenous DCs was necessary for contact hypersensitivity responses.

240 of P-selectin expression leads to decreased contact hypersensitivity responses.

241 plotype mice developed significantly greater contact-hypersensitivity responses to DMBA than H-2(b),

242 otic naive mice with L. major or testing for contact hypersensitivity results in exacerbated skin inf

243 In a multiple challenge model of contact hypersensitivity, rolling of Tregs and conventio

244 Chronic contact hypersensitivity skin of Sash mice exhibited ele

245 d, LC depletion in one model led to enhanced contact hypersensitivity, suggesting they play a negativ

246 ated inflammatory responses in two models of contact hypersensitivity that exhibit features of allerg

247 xposure protected against suppression of the contact hypersensitivity that is a hallmark of ultraviol

248 radiation (SSR) on the elicitation phase of contact hypersensitivity to 2,4-dinitrochlorobenzene (DN

249 uld suppress in IL-10T mice the induction of contact hypersensitivity to a hapten applied to the skin

250 logeneic cells upon challenge but had normal contact hypersensitivity to an epicutaneously applied ha

251 We used a standard murine model of contact hypersensitivity to determine whether chronic AC

252 Generation of contact hypersensitivity to dinitrofluorobenzene, which

253 e the predominant effector cells in allergic contact hypersensitivity to DMBA and that CD4(+) T cells

254 In CD8 knockout (CD8(-/-)) mice, allergic contact hypersensitivity to DMBA was reduced compared wi

255 injection of EPI inhibited the induction of contact hypersensitivity to epicutaneously administered

256 waveband dependencies for the suppression of contact hypersensitivity to oxazolone and delayed-type h

257 altered innate and humoral responses (e.g., contact hypersensitivity to oxazolone, IgM response to P

258 s measured by the inhibition of delayed type contact hypersensitivity to the chemical dinitrofluorobe

259 could not detect a role in the induction of contact hypersensitivity to various doses of hapten.

260 During contact hypersensitivity, VEGFR-3, CCL21, and HS express

261 No contact hypersensitivity was induced in mice lacking all

262 Paradoxically, T cell-mediated allergic contact hypersensitivity was severely attenuated in CD39

263 In contrast, contact hypersensitivity was unaffected, suggesting that

264 he suppressive influence of ultraviolet-B on contact hypersensitivity, we compared the effects of top

265 ential roles of CD4+ and CD8+ T cells during contact hypersensitivity, we examined the T-cell-depende

266 In a mouse model of contact hypersensitivity, we found that a non-Fc recepto

267 hin LCs was associated with an alteration in contact hypersensitivity, we treated mice with only a si

268 L-1beta has been shown to play a key role in contact hypersensitivity; we show that ASC- and NALP3-de

269 and hypersensitivity as well as delayed-type contact hypersensitivity were attenuated in Spns2(-/-) m

270 with molecules designed to abort or prevent contact hypersensitivity when it causes disease.

271 al lymphatic vessels of mice exposed to skin contact hypersensitivity where they mediate lymph node t