ライフサイエンスコーパス: allergen exposure

1 o oxidative stress) and BALB/C (sensitive to allergen exposure).

2 es persisted for 6 months after cessation of allergen exposure.

3 odulating Th2 inflammation following mucosal allergen exposure.

4 exposure and poor antioxidant response after allergen exposure.

5 ed by Th2-cell-type cytokines in response to allergen exposure.

6 el spontaneously resolves after cessation of allergen exposure.

7 ional and environmental (indoor and outdoor) allergen exposure.

8 nophils recruited and activated by pulmonary allergen exposure.

9 egulatory cells, exaggerated with additional allergen exposure.

10 was increased in waved-2 mice skin following allergen exposure.

11 accumulation in AD skin following cutaneous allergen exposure.

12 te units for the assessment of environmental allergen exposure.

13 n Baltimore should prioritize reducing mouse allergen exposure.

14 -fat- or high-fructose-fed mice even without allergen exposure.

15 and inflammation following acute and chronic allergen exposure.

16 t is unknown whether pollen counts represent allergen exposure.

17 s were detectable in the lungs after chronic allergen exposure.

18 s to public health associated with increased allergen exposure.

19 velopment of eosinophilic inflammation after allergen exposure.

20 gic inflammation in the absence of exogenous allergen exposure.

21 s expressed on lung inflammatory cells after allergen exposure.

22 h to study effectively how AD is affected by allergen exposure.

23 lic inflammation, and IL-13 levels following allergen exposure.

24 e that later primes the esophagus on further allergen exposure.

25 ing the migration of Th2 cells into sites of allergen exposure.

26 tion, particularly in the setting of ongoing allergen exposure.

27 nse-but only if participants had slept after allergen exposure.

28 at are differentially expressed after airway allergen exposure.

29 development of lung pathology in response to allergen exposure.

30 d CXCL13) were increased only after a second allergen exposure.

31 ed airway inflammation and obstruction after allergen exposure.

32 the resolution of MCM following cessation of allergen exposure.

33 d asthma among children with a wide range of allergen exposure.

34 ss-switching of B-cells to produce IgE after allergen exposure.

35 hese cells substantially increase after oral allergen exposure.

36 lability for recruitment to the airway after allergen exposure.

37 ent of in vivo allergic responses to inhaled allergen exposure.

38 oth T cell and NK cell populations following allergen exposure.

39 This difference was independent of allergen exposure.

40 s is a life-threatening complication of food allergen exposure.

41 se phenotype after 48 h, 1, 3, or 5 weeks of allergen exposure.

42 3-LD, SYN-4, or placebo, followed by a final allergen exposure.

43 ad to life-threatening anaphylaxis following allergen exposure.

44 sinophilia following chronic house dust mite allergen exposure.

45 fic IgE production and anaphylaxis following allergen exposure.

46 ase crucial inflammatory mediators following allergen exposure.

47 ergies through incremental increases in oral allergen exposure.

48 D8(+) T(RM) cells to the epidermis following allergen exposure.

49 roduction occurred at 6 months and reflected allergen exposure.

50 in early life to induce persistent AHR after allergen exposure.

51 ay is involved in the Tfh response to peanut allergen exposure.

52 sthma are modified by the level of dust mite allergen exposure.

53 production in NT4(-/-) mice after early life allergen exposure.

54 t data variability secondary to inconsistent allergen exposure.

55 eosinophilopoiesis in the bone marrow after allergen exposure.

56 ributing to epithelial wall damage following allergen exposure.

57 d in the airways of asthmatic patients after allergen exposure.

58 s led to exacerbated lung inflammation after allergen exposure.

59 ges in the airways following chronic inhaled allergen exposure.

60 and no rise in serum IgE after multiple HDM-allergen exposures.

61 res and have often lacked well-characterized allergen exposures.

62 ficacy for controlling clinical responses to allergen exposures.

63 o induce type 2 immune responses to repeated allergen exposures.

64 correlates with allergen dose and number of allergen exposures.

65 lergy, a risk often attributed to cow's milk allergens exposure.

66 y changes at the small molecule level due to allergen exposure, (2) determine perturbed pathways due

67 esponse ratio was significantly higher after allergen exposure (57 mg/% FEV1 fall [27-121] to 147 mg/

68 cognized that the timing, load, and route of allergen exposure affect allergic disease phenotypes and

69 as influenced by asthmatic status, levels of allergen exposure, age, race-ethnicity and smoking statu

70 Following neonatal allergen exposure, allergen-specific T(H)2-TRMs were tra

71 veloped AHR and some lung eosinophilia after allergen exposure alone and when RSV infection preceded

72 T(FH) accumulated with sustained allergen exposure, alongside germinal centre (GC) B cell

73 Allergen exposure also induces acute extracellular accum

74 ded peripheral Treg cells, while concomitant allergen exposure altered the phenotype of expanded Treg

75 SPDEF was induced following intratracheal allergen exposure and after Th2 cytokine stimulation and

76 een the lungs and bone marrow, we used acute allergen exposure and airway inflammation models in mice

77 that the dose-response relationship between allergen exposure and allergic disease may differ betwee

78 mber (EEC) was used to reduce variability of allergen exposure and allow investigation of symptom red

79 increased quickly within several hours after allergen exposure and continued to rise throughout the c

80 ergic type 2 immune responses on respiratory allergen exposure and counteracts the Th2 priming effect

81 showed reduced lung pathology after chronic allergen exposure and decreased type 2 cytokine producti

82 Group 2 ILCs (ILC2s) respond rapidly to allergen exposure and environmental insults in mucosal o

83 ewly identified allergens reflect globalized allergen exposure and growing research activities outsid

84 s induced by environmental challenge chamber allergen exposure and had a favorable safety profile.

85 igning costly and labor-intensive studies of allergen exposure and health outcomes, commonly used in

86 ell as the body of evidence on environmental allergen exposure and how this can sensitize an individu

87 mucosal cytokine responses induced by nasal allergen exposure and humoral immune responses that incl

88 ned genes modulated in concomitance with the allergen exposure and inhibition of responses in non-all

89 develop quickly in lung tissue after initial allergen exposure and persist for a prolonged period.

90 ed with oxidative stress in the lungs before allergen exposure and poor antioxidant response after al

91 o in human subjects, oxidative stress before allergen exposure and poor antioxidant responses were as

92 from indoor environments in order to assess allergen exposure and possible relationships to health o

93 cells are rapidly recruited to the lung upon allergen exposure and release eotaxins that coordinately

94 In allergic rhinitis, initial allergen exposure and sensitization involves antigen-pre

95 on mutations modify the relationship between allergen exposure and sensitization, but effects differ

96 The relationship between dose of allergen exposure and symptom severity is unclear.

97 of asthma, but the relationship between the allergen exposure and the bronchial symptoms has not bee

98 ules is profoundly dependent on the route of allergen exposure and the child's IgE sensitization stat

99 n AR individuals, including the avoidance of allergen exposure and the pharmacotherapy.

100 Allergen exposure and the resulting symptoms vary, and t

101 tion of T(FH) to disease during chronic aero-allergen exposure and the therapeutic potential of targe

102 Environmental assessments included allergen exposure and, in a nested case-control study of

103 Rationale: The relationships between allergen exposures and allergy and asthma are complex.

104 t underlie the synergistic interplay between allergen exposures and viral infections.

105 vironmental tobacco smoke exposure, obesity, allergen exposure, and availability of health care.

106 leased quickly by airway epithelial cells on allergen exposure, and it plays an important role in typ

107 t eosinophils express CAR4 following IL-5 or allergen exposure, and that CAR4 is involved in regulati

108 thickness were increased following cutaneous allergen exposure, and these were further enhanced in th

109 Atopy, mite allergen exposure, and vitamin D levels were also measur

110 ze (maternal smoking, breast-feeding, indoor allergen exposures, and lower respiratory infections).

111 Although environmental factors such as allergen exposure are risk factors in the development of

112 Conclusions: Allergen exposures are common in COPD and associated wit

113 Certain environmental allergen exposures are more common in disadvantaged comm

114 By utilizing cutaneous allergen exposure as a model, this review explores the p

115 Allergen exposure at lung and gut mucosae can lead to ab

116 d a temporary association between higher HDM allergen exposure at the age of 3 months and more asthma

117 impact of concurrent influenza infection and allergen exposure at the genomic level, using whole-geno

118 Management includes allergen exposure avoidance or reduction (second best op

119 ity of predicting and determining individual allergen exposure because of many factors (eg, pollen se

120 ifferences were observed in MCM at 5 days of allergen exposure between +/+ and -/- mice, despite redu

121 ing and breast-feeding behaviors, as well as allergen exposure, birth weight, and lower respiratory i

122 rigger degranulation of mast cells following allergen exposure, but also to enhance their survival.

123 Mouse allergen exposure, but not other indoor exposure, was as

124 hat healthy individuals are not oblivious to allergen exposure, but rather react with an active modul

125 TRM in the lungs do respond to a subsequent allergen exposure by decreasing expression of the transc

126 chronic allergic asthma, we mimicked natural allergen exposure by giving tiny doses of dust-mite extr

127 ole in mucus overproduction after early life allergen exposure by orchestrating PNEC innervation and

128 Mucosal grass pollen allergen exposure by SLIT resulted in highly diverse IgE

129 in of IgE memory responses following mucosal allergen exposure by sublingual immunotherapy (SLIT) wer

130 Following passive sensitization and allergen exposure, C57BL/6+/+ mice developed altered air

131 Long-term allergen exposure can attenuate inflammation and revert

132 Allergen exposure can confound the management of asthma.

133 Inflammatory responses induced by allergen exposure cause mucous cell metaplasia (MCM) by

134 Longitudinal evidence that indoor allergen exposure causes morbidity in sensitized individ

135 gE ASC production continued for months after allergen exposure ceased.

136 Allergen exposure chamber (AEC) is a clinical facility t

137 An allergen exposure chamber (AEC) is a specialized medical

138 Following baseline exposure in an allergen exposure chamber (AEC), 166 subjects were rando

139 ing the efficacy of sublingual tablets in an allergen exposure chamber over a 4-month period.

140 ives to conventional field trials, including allergen exposure chamber studies are still to be elucid

141 subjects were exposed to grass pollen in an allergen exposure chamber.

142 e III (field) studies and the future role of Allergen Exposure Chambers (AEC) in AIT product developm

143 Allergen exposure chambers (AECs) are clinical facilitie

144 levated in Bax -/- mice following 15 days of allergen exposure compared with +/+ mice, while the numb

145 an increase in capsaicin-evoked coughs after allergen exposure compared with diluent at both 30 minut

146 Bedroom allergen exposures contribute to allergic disease morbid

147 leukotrienes phenocopied the WT response to allergen exposure; conversely, anti-PlGF Ab administrati

148 emic or mucosal administration of ISS before allergen exposure could provide a novel form of active i

149 ctivity, suppressed as a result of long-term allergen exposure, could be reestablished by depleting g

150 Subsequent allergen exposure cross-links mast cell-bound IgE, resul

151 Following allergen exposure, cytokines and other pro-inflammatory

152 evels to exogenous allergens were boosted by allergen exposure, declined thereafter, and seemed to be

153 uces IgE synthesis by B cells in response to allergen exposure, decreases the expression of IgE recep

154 Whereas OVA allergen exposure did not induce inflammation in WT cont

155 Dog allergen exposure did not show such interaction.

156 At a high level, initial allergen exposure disrupts epithelial integrity, trigger

157 cepsilonRI complexes that prime cells before allergen exposure dissociate extremely slowly and cannot

158 cates that oxidative stress condition before allergen exposure due to an inadequate antioxidant respo

159 glected safety issues associated to possible allergen exposure due to the newly proposed bio- and pla

160 Indoor environmental allergen exposure during early life can also affect dise

161 lacebo-controlled field studies with natural allergen exposure during the allergen season.

162 We investigated the effect of maternal allergen exposures during pregnancy on allergen-induced

163 In our model, maternal allergen exposures during pregnancy prevented later alle

164 memory (CD62L(hi)) subsets, which vary with allergen exposure (e.g., during, or out with, pollen sea

165 Early life allergen exposure elevated the level of NT4 and caused P

166 climate change in the context of plants and allergen exposure, emphasizing direct effects on plant p

167 e the magnitude of effect in an uncontrolled allergen exposure environment.

168 After cessation of allergen exposure, eosinophils and T cells were cleared

169 After 5 days of allergen exposure, extensive MCM had developed but was r

170 ion as an appropriate alternative to natural allergen exposure for AIT product efficacy assessment.

171 After allergen exposure, GCs that form in the lung are much sm

172 Prenatal allergen exposure has been linked to both induction and

173 not single phenotypes, and it is likely that allergen exposure has different effect on distinct subgr

174 After allergen exposure, HDM-specific memory cells persisted a

175 he first time, we have shown that on mucosal allergen exposure, human IgE memory resides in allergen-

176 ase in childhood food allergy (FA), the dual-allergen exposure hypothesis has been the most extensive

177 ternative route of sensitization in the dual allergen exposure hypothesis that leads to food allergy.

178 ood allergy is that in keeping with the dual allergen exposure hypothesis, barrier- and immune-relate

179 tion and how this forms one half of the dual-allergen exposure hypothesis.

180 RNA-seq analysis following allergen exposure identified a network of pro-inflammato

181 f dopamine-DRD4 signaling following neonatal allergen exposure impairs lung residence of T(H)2 cells

182 CM levels were decreased 4-fold at 7 days of allergen exposure in -/- mice and at 15 days in +/+ mice

183 ive hypersensitivity responses to subsequent allergen exposure in an allergen-specific manner, effect

184 Pulmonary allergen exposure in C5aR-targeted mice resulted in incr

185 Standardized allergen exposure in challenge chamber settings might be

186 data define the importance of age at initial allergen exposure in dictating subsequent responses in t

187 l drawbacks, such as the high variability of allergen exposure in different trial sites or seasons an

188 Allergic asthma develops from allergen exposure in early childhood and progresses into

189 It is unclear whether the initial route of allergen exposure in early life could influence the subs

190 lia, eosinophilic esophagitis was induced by allergen exposure in IL-5-deficient and wild-type mice.

191 Chronic allergen exposure in mice resulted in increased density

192 a gene deficiency were studied in a model of allergen exposure in mice sensitised and challenged with

193 under the curve for the first 3 hours after allergen exposure in NAC or after initiation of exposure

194 We found that allergen exposure in neonatal mice, but not in adult mic

195 unotherapy (AIT) mediates protection against allergen exposure in part due to allergen-specific antib

196 of eotaxin mRNA are known to increase after allergen exposure in sensitized animals.

197 RATIONALE: Allergen exposure in sensitized individuals with asthma

198 vivo role of IL-12 in the immune response to allergen exposure in susceptible (A/J) and resistant (C3

199 Clinical endpoints assessed to allergen exposure in the AEC and NAC significantly corre

200 The role of allergen exposure in the development of allergic disease

201 arch to elucidate the role of chronic indoor allergen exposure in the development of glaucomatous opt

202 OSS) were assessed every 15 min during a 4-h allergen exposure in the Vienna Challenge Chamber.

203 enitors of goblet cells induced by pulmonary allergen exposure in vivo.

204 conducting airway epithelium after pulmonary allergen exposure in vivo.

205 nd climatic factors, associated with bedroom allergen exposures in a nationally representative sample

206 stic interplay between respiratory virus and allergen exposures in the onset and progression of asthm

207 or monitoring environmental and occupational allergen exposure including sampling strategies and meth

208 lung and draining lymph nodes revealed that allergen exposure increased TREM-2 expression on all DC

209 Our study supports the hypothesis that early allergen exposure increases tolerance and lowers risk of

210 ch as breastfeeding, antibiotic use and food allergen exposure, indicate the first year of life in ch

211 Allergen exposure induced Serpinb3a expression in the sk

212 are present in allergic subjects and (2) cat allergen exposure induces an IgG4 response in a TH2 cell

213 We propose that allergen exposure induces elevation in SP-D protein leve

214 Allergen exposure induces the airway epithelium to produ

215 Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscen

216 n 5 French regions according to the route of allergen exposure (inhaled vs food allergens).

217 Allergen exposure is associated with the development of

218 he time interval between viral infection and allergen exposure is critical in determining whether vir

219 vation through the alternative pathway after allergen exposure is critical to the development of AHR

220 chanism underlying IL-33 secretion following allergen exposure is not clear.

221 This synergy between DEP and natural allergen exposure is suggested as a key feature in incre

222 Ms in the immature lung following early life allergen exposure is unknown.

223 neighborhood-level air pollution and indoor allergen exposure, lack of transportation to medical app

224 These data suggest that repeated allergen exposure leads to progressive decreases in AHR

225 The allergenicity of a food protein, allergen exposure levels, and atopy are important risk f

226 Our current observations suggest that allergen exposure may contribute to poor asthma control

227 t use of COX-inhibiting drugs during initial allergen exposure may increase the risk of developing al

228 tial period of bronchoconstriction following allergen exposure may involve neither mast cells nor IgE

229 uman epidemiologic studies suggest high-dose allergen exposure may paradoxically protect against sens

230 Cockroach and mouse, but not dog or cat, allergen exposure may predispose children with asthma to

231 ence with CD28-mediated costimulation during allergen exposure might be an attractive therapeutic con

232 We have developed a novel chronic allergen exposure model using the clinically relevant an

233 in the healthy immune response to high-dose allergen exposure models in humans, T regulatory cells a

234 Dust mite allergen exposure modifies the estimated effect of rs117

235 In mixed models, allergen exposure modulated (q </= 0.2) miRNAs including

236 tly, marked airway hyperreactivity only when allergen exposure occurred during an acute influenza A i

237 h2 responses to allergens, particularly when allergen exposure occurs concomitantly with exposure to

238 -VLA-4 and anti-IL-5 in a model of secondary allergen exposure of previously sensitized and challenge

239 The effect(s) of allergen exposure on airway responsiveness to indirect-a

240 We sought to investigate the effects of allergen exposure on cough reflex sensitivity.

241 f this study was to determine the effects of allergen exposure on leukotriene generation and inflamma

242 s-of-function mutations modify the effect of allergen exposure on the development of allergic sensiti

243 the present study, we examined the effect of allergen exposure on TREM-2 expression in the airways an

244 tolerance has been observed after high-dose allergen exposure or after completed allergen immunother

245 It is currently unknown why allergen exposure or environmental triggers in patients

246 Other factors such as timing of allergen exposure or other environmental adjuvants may c

247 en participants stayed awake the night after allergen exposure or were tested in a different context.

248 signaling was antagonized concomitantly with allergen exposure, or the development of allergic airway

249 After allergen exposure, or upon treatment of naive lung cells

250 ticosteroid use, but not atopic status, mite allergen exposure, or vitamin D levels, modified the ass

251 Susceptibility to allergen exposure, other environmental exposures and the

252 ays in regulating immunological tolerance to allergen exposure outside the GI tract and proposes the

253 Cumulative allergen exposure over the first 3 years was associated

254 be predictive of symptom severity upon grass allergen exposure (P = 0.029).

255 s that serve as a rapid source of IL-13 upon allergen exposure play a major role in Tfh cell developm

256 Eos recruited to the airways after allergen exposure produce and respond to IL-5 and GM-CSF

257 ate that elevated levels of IL-5 and mucosal allergen exposure promote eotaxin-dependent eosinophil t

258 (such as passive or active smoking, ongoing allergen exposure, psychosocial factors) have to be a pr

259 We sought to determine whether mouse allergen exposure reduction is associated with lung func

260 g acute stress and inflammatory responses to allergen exposure remain poorly understood.

261 that leads to IgG4 induction during chronic allergen exposure remains poorly understood.

262 ti-CD3 F(ab')2 administration at the time of allergen exposure represents a viable strategy for limit

263 Allergen exposure resulted in airway recruitment of Gal-

264 t numbers, even in the context of continuous allergen exposure, resulting in improved lung function.

265 vations in both mice and humans suggest that allergen exposure results in increased output of eosinop

266 After allergen exposure, rhinovirus-induced neutrophilic and e

267 ce in children in the presence or absence of allergen exposure/sensitization in the Cincinnati Childh

268 l models that closely mimic natural modes of allergen exposure should prove most informative.

269 allergies, nasal symptoms, and environmental allergen exposure significantly associated with LPR.

270 Following allergen exposure, ST2(+) T(reg) cells were activated by

271 ajor cat allergen Fel d 1 has been shown, in allergen exposure studies, to significantly reduce sympt

272 esponsible for Th2 sensitization at sites of allergen exposure, such as airway and skin, is crucial f

273 Some aspects of work-related allergen exposure, such as route and frequency of exposu

274 recruitment to the lungs of asthmatics after allergen exposure suggests platelets participate in vari

275 oduction of IgE antibodies in the absence of allergen exposure suggests the existence of long-lived I

276 ly inflammatory response following cutaneous allergen exposure, supporting a role for Serpinb3a (mice

277 Concurrent viral infection and allergen exposure synergistically increase exacerbation

278 rved in human subjects as the consequence of allergen exposures that recurrently activate memory B ce

279 In murine models of allergen exposure, the dopamine-DRD4 pathway augmented T

280 ms in patients with allergies resulting from allergen exposure, there are few preventive therapies ot

281 Allergic airway inflammation is triggered by allergen exposure through several steps including releas

282 onse in peanut-tolerant groups suggests that allergen exposure through the GI tract induces tolerance

283 ding to the individual atopic propensity and allergen exposure, thus producing an extreme heterogenei

284 postnatal growth, thereby linking early-life allergen exposure to persistent airway dysfunction.

285 We sought to determine whether exposure to allergen, exposure to diesel exhaust (DE), or coexposure

286 a, prior to sensitization, challenge, or all allergen exposures, to assess the role of oxidative stre

287 im to operate with a stable and reproducible allergen exposure under highly standardized environmenta

288 Allergen exposure upregulated IL-25 and induced type 2 c

289 Allergen exposure was also associated with an increase i

290 Allergen exposure was defined as dog or cat in the home

291 fer repeated relapses caused by intermittent allergen exposure, we hypothesized that allergen- specif

292 Using a model of cutaneous allergen exposure, we show that allergens directly activ

293 eosinophilia and AHR after RSV infection and allergen exposure were also markedly reduced.

294 ermore, early and late phases resulting from allergen exposure were shown to involve similar lung reg

295 ch measures to reduce prenatal and postnatal allergen exposure were undertaken (active HRA) (n=145) o

296 Early cockroach, mouse, and cat allergen exposures were significantly associated with se

297 ed increased CCR5 expression after high-dose allergen exposure while CXCR4, CXCR5, CCR6, and CCR7 exp

298 and interaction of environmental, viral, and allergen exposures with immune pathways that impact dise

299 xhibited increased airway inflammation after allergen exposure, with massive eosinophilic lung infilt

300 Allergen exposure worsens viral-triggered asthma exacerb