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

1 suppression of both CD8 T cell expansion and 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 draining lymph nodes following induction of contact hypersensitivity.

9 a distant site also suppressed induction of contact hypersensitivity.

10 regulate keratinocyte function and death in contact hypersensitivity.

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

12 pathophysiology of the elicitation phase of contact hypersensitivity.

13 use of the lack of murine models for chronic 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 ning protocol to a rat model of DNFB-induced contact hypersensitivity.

19 portant but distinct role in the 2 phases of contact hypersensitivity.

20 form skin inflammation and cutaneous delayed contact hypersensitivity.

21 atory function in models of autoimmunity and contact hypersensitivity.

22 ed skin of mice undergoing oxazolone-induced contact hypersensitivity.

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

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

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

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

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

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

29 utaneous application of ovalbumin and during contact hypersensitivity.

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

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

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

33 ore severe inflammation in oxazolone-induced contact hypersensitivity, a model of atopic dermatitis.

34 In an acute mouse model of contact hypersensitivity, a murine surrogate anti-TNF-GR

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

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

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

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

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

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

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

42 In vivo mouse models of contact hypersensitivity and ex vivo models of human ski

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

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

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

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

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

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

49 stasis and atopic dermatitis associated with contact hypersensitivity and type 2 inflammation.

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

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

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

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

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

55 nding plays a role in mediating DNCB-induced contact hypersensitivity, and the activation of CD91 by

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

57 lymphatics separately in the 2 phases, using contact hypersensitivity as a model of human allergic in

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

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

60 Contact hypersensitivity assay (CHS) faithfully models h

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

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

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

64 In a mouse model of contact hypersensitivity, beta-arrestin-biased CXCR3-med

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

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

67 r Treg behavior, whereas 48 h after inducing contact hypersensitivity by oxazolone challenge, CD103 i

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

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

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

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

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

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

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

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

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

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

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

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

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

81 RBC) leads to hapten-specific suppression of contact hypersensitivity (CHS) in mice, mediated by ligh

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

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

84 h2-dependent skin inflammation in a model of contact hypersensitivity (CHS) induced by the hapten flu

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

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

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

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

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

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

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

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

93 Contact hypersensitivity (CHS) of murine skin serves as

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

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

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

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

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

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

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

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

102 Contact hypersensitivity (CHS) requires activation of th

103 Dock8(-/-) mice demonstrated an exaggerated contact hypersensitivity (CHS) response to oxazolone wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 10-deficient (IL-10(-/-)) mice have enhanced contact hypersensitivity (CHS) to topical hapten.

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

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

121 Neutrophils are essential during contact hypersensitivity (CHS), a common skin allergic d

122 -12 play a pivotal role in the initiation of contact hypersensitivity (CHS), a Th1 immune response in

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

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

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

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

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

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

129 induced immunotolerant program in a model of contact hypersensitivity (CHS).

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

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

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

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

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

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

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

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

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

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

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

141 In contact hypersensitivity, collagen-induced arthritis, an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 CGRP receptor antagonist similarly inhibited contact hypersensitivity in wild-type mice.

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

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

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

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

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

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

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

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

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

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

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

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

175 Contact hypersensitivity induction was impaired in ultra

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

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

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

179 Contact hypersensitivity is a CD8 T cell-mediated respon

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

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

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

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

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

185 effects of IL-26 were observed in the murine contact hypersensitivity model, indicating that these ef

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

187 In the contact hypersensitivity model, this was associated with

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

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

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

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

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

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

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

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

196 Finally, using a murine model of contact hypersensitivity, PDT immunosuppression was bloc

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

198 Although murine contact hypersensitivity provides a framework for unders

199 on of CD83 expression resulted in aggravated contact hypersensitivity reaction accompanied by enhance

200 lls accumulated in the skin during the acute contact hypersensitivity reaction and gave rise to epide

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

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

203 d(del) and control mice developed comparable contact hypersensitivity reactions and imiquimod-trigger

204 Contact hypersensitivity reactions in response to variou

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

206 We found that contact hypersensitivity reactions to oxazolone in mice

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

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

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

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

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

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

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

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

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

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

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

218 Allergic contact hypersensitivity response to oxazolone and oxazo

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

220 Contact hypersensitivity response was evaluated by measu

221 The contact hypersensitivity response was significantly supp

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

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

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

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

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

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

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

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

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

231 Contact hypersensitivity responses (CHS) to dinitrochlor

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

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

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

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

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

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

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

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

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

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

242 Ear swelling chronic contact hypersensitivity responses increased markedly, u

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

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

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

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

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

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

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

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

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

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

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

254 Contact hypersensitivity responses were acquired by such

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

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

257 AMP1 knockout mice had significantly reduced contact hypersensitivity responses, and systemic adminis

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

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

260 erance induction to hapten sensitization and contact hypersensitivity responses.

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

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

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

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

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

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

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

268 Chronic contact hypersensitivity skin of Sash mice exhibited ele

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

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

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

272 1-chloro-2,4-dinitrobenzene (DNCB), elicits contact hypersensitivity through binding the protein we

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

274 We used an experimental model of ACD (ie, contact hypersensitivity to 2,4-dinitrofluorobenzene) th

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

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

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

278 Contact hypersensitivity to dinitrofluorobenzene was exa

279 Generation of contact hypersensitivity to dinitrofluorobenzene, which

280 d IL-13 inhibited the T(H)1 cell response in contact hypersensitivity to dinitrofluorobenzene.

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

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

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

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

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

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

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

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

289 Contact hypersensitivity was attenuated in catalytically

290 No contact hypersensitivity was induced in mice lacking all

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

292 In contrast, contact hypersensitivity was unaffected, suggesting that

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

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

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

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

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

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

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

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