ライフサイエンスコーパス: allergic

1 ble; 43 (24%) received testing and none were allergic.

2 These data show the lowest rate of immediate allergic adverse events with use of the nonionic linear

3 ammatory responses during the development of allergic airway disease (AAD).

4 albumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were dev

5 ive cell transfer studies in mouse models of allergic airway disease, we examined the effects of Act-

6 ntioxidants and NOX inhibitors in mitigating allergic airway disease.

7 th PC receptors in the lung protects against allergic airway disease.

8 pollution (TRAP) exposure is associated with allergic airway diseases and reduced lung function in ch

9 ls was dispensable for successful therapy of allergic airway inflammation (AAI) with dexamethasone.

10 The pathology of ovalbumin-induced acute allergic airway inflammation after adoptive transfer of

11 and Wnt pathways during early- or late-onset allergic airway inflammation and to address regulatory m

12 T sera with IgE-blocking activity ameliorate allergic airway inflammation in a human/mouse chimeric m

13 D138(+)IL-10(+) cells dramatically decreased allergic airway inflammation in wild-type and Sema4c(-/-

14 These novel observations suggest that allergic airway inflammation increases FAO in inflammato

15 Allergic airway inflammation is triggered by allergen ex

16 tant DEP+HDM exposure significantly enhanced allergic airway inflammation, as characterized by increa

17 we report that, during cockroach Ag-induced allergic airway inflammation, Foxp3(+) Tregs are rapidly

18 rophylactic or therapeutic Syk inhibition on allergic airway inflammation, hyperresponsiveness, and a

19 Using a mouse model of allergic airway inflammation, we found that adoptive tra

20 icated as central immune modulator promoting allergic airway inflammation.

21 mice, resulting in an impaired DEP-enhanced allergic airway inflammation.

22 gulation in a mouse model of house dust mite allergic airway inflammation.

23 erve to limit ILC2 activation and subsequent allergic airway inflammation.

24 the lung and lymph nodes in murine model of allergic airway inflammation.

25 flammation/remodeling in long term models of allergic airway inflammation.

26 IL-33 signaling are regulated by miR-155 in allergic airway inflammation.

27 ffect of Cavbeta antisense and gabapentin in allergic airway inflammation.

28 and TC may occur as an early event promoting allergic airway inflammation.

29 lymphocytes and on the development of acute allergic airway inflammation.

30 ave been linked mechanistically in models of allergic airways disease and have been associated with a

31 Rho kinases (ROCKs) contribute to allergic airways disease.

32 r HDM-induced glycolysis and pathogenesis of allergic airways disease.

33 of susceptibility to fungal allergen-induced allergic airways disease.

34 the ability of adoptive transfer to restore allergic airways inflammation in ROCK2-insufficient mice

35 ROCK2 contributes to allergic airways responses likely via effects within ASM

36 Allergic airways responses were measured 48 h after the

37 role of ROCK2 acting within CD4(+) cells in allergic airways responses.

38 Skin microbiota can impact allergic and autoimmune responses, wound healing, and an

39 ctivities in these patients compared to food-allergic and control patients.

40 he new classification model addressed to the allergic and hypersensitivity conditions according to th

41 ssociation of currently used pesticides with allergic and non-allergic wheeze among male farmers.

42 cimens (n = 68) from 52 highly characterized allergic and nonallergic children (0.5-17 years) with se

43 therapies for the prevention or treatment of allergic and other inflammatory diseases.

44 gents already approved for the management of allergic and respiratory disorders and biologics current

45 In the United States, the prevalence of allergic asthma (AA) is inexplicably rising and in utero

46 e treatment of moderate-to-severe persistent allergic asthma (AA) that remains uncontrolled despite h

47 al cause of allergic rhinoconjunctivitis and allergic asthma and has the potential to alter the natur

48 The number of patients suffering from allergic asthma and rhinoconjunctivitis has increased dr

49 Allergic asthma is a chronic lung disease resulting from

50 Allergic asthma is a chronic Th2 inflammation in the lun

51 Allergic asthma is a significant health burden in wester

52 Allergic asthma is characterized by inflammation and air

53 oal was to delineate a mechanism(s) by which allergic asthma may alleviate influenza disease outcome,

54 ify Sema3E as a novel regulatory molecule in allergic asthma that acts upstream of proallergic events

55 Allergic asthma was induced in C57BL/6 J wild-type mice,

56 In a murine model of allergic asthma, glycolysis was induced in the lungs in

57 In allergic asthma, inhalation of airborne allergens such a

58 In this experimental model of allergic asthma, matched bronchoalveolar lavage (BAL) fl

59 molecule could be a novel approach to treat allergic asthma.

60 ouse model of severe exacerbation of chronic allergic asthma.

61 the relevance of glycolysis in patients with allergic asthma.

62 f NSC23766 prevented AHR in murine models of allergic asthma.

63 ibody, is used to treat patients with severe allergic asthma.

64 allergic patients and in peripheral blood of allergic asthmatic patients.

65 Sputum basophil numbers are increased in allergic asthmatics, but it is unclear what role airway

66 T cells that are heavily implicated in human allergic, autoimmune, and malignant diseases.

67 Thereafter, allergic behaviour of this glycated protein was compared

68 Nasal levels of selected allergic biomarkers demonstrated trends for reductions a

69 netic resonance (MR) imaging to discriminate allergic bronchopulmonary aspergillosis (ABPA) in cystic

70 The diagnosis of allergic bronchopulmonary aspergillosis relies on criter

71 isms (tag SNPs) in 367 challenge-proven food allergic cases, 199 food-sensitized tolerant cases and 1

72 y naturally resolves in a proportion of food-allergic children without intervention; however the unde

73 ting an impaired mucosal barrier function in allergic children.

74 ographical areas with relevant allergens and allergic clinical picture.

75 ficantly reduced odds of both atopy and "any allergic condition" (adjusted OR AOR, 95% CI, 0.54; 0.32

76 tly, related to prevalence of atopy and "any allergic condition" at age 6.5 years.

77 omorbidities extend well beyond the march to allergic conditions (food allergy, asthma, allergic rhin

78 It is well recognized that knowledge of allergic conditions is suboptimal in primary care.

79 ylori is inversely associated with atopy and allergic conditions.

80 ns (food allergy, asthma, allergic rhinitis, allergic conjunctivitis, and eosinophilic esophagitis),

81 t for CCL7 in a murine model of IgE-mediated allergic conjunctivitis.

82 ce to haptens is an efficient way to prevent allergic contact dermatitis (ACD) in mice.

83 nd inflammation are commonly associated with allergic contact dermatitis (ACD), it is not known if th

84 levance of SUCNR1/GPR91 expression mediating allergic contact dermatitis (ACD).

85 e a potential therapeutic avenue in treating allergic contact dermatitis.

86 d patients with SAR (n = 41) and healthy non-allergic controls (n = 42) performed a dual-task paradig

87 d-sensitized tolerant cases and 156 non-food allergic controls from the HealthNuts study.

88 pulation-based cohort, the prevalence of any allergic disease among 4-year-old children in Melbourne,

89 iation between S. aureus carriage and severe allergic disease and allergic multimorbidity.

90 portant knowledge gaps regarding its role in allergic disease and delineating strategies necessary to

91 UFA levels in colostrum and breast milk with allergic disease and lung function at ages 12 and 18 yea

92 There were no differences in allergic disease between LEAP groups.

93 tion-based cohort experienced symptoms of an allergic disease in the first 4 years of their life.

94 damp indoor environments is associated with allergic disease in young children, but it is unclear wh

95 upports the role of ambient air pollution in allergic disease inception.

96 licated in the development and regulation of allergic disease independent of their antibody reactivit

97 ly assumed that the contribution of fungi to allergic disease is mediated through their potent antige

98 The antibody IgE plays a central role in allergic disease mechanisms.

99 concentration of breast milk fatty acids and allergic disease outcomes were included.

100 Allergic disease phenotypes were defined by using questi

101 vides the basis for an alternative target in allergic disease therapy.

102 of parental clinical outcome with offspring allergic disease were estimated with multinomial logisti

103 methylation at birth and the development of allergic disease, we examined the methylation status of

104 the potential to alter the natural course of allergic disease.

105 he type 2 immune responses that characterize allergic disease.

106 ch is the primary causal factor in childhood allergic disease.

107 ing, and still there is a high prevalence of allergic disease.

108 ng use of anti-IgE mAbs for the treatment of allergic disease.

109 have been few studies on antibiotic use and allergic disease.

110 The prevalence of allergic diseases and asthma has dramatically increased

111 t option in almost two-third of all types of allergic diseases and in 90% of individuals suffering fr

112 ys are most important in the pathogenesis of allergic diseases and in the development of symptoms and

113 nsitization and high frequencies of comorbid allergic diseases are characteristic of severe asthma in

114 r, clinical studies with bacteria to prevent allergic diseases are still rare and to some extent cont

115 Allergic diseases caused by fungi are common.

116 ns, whereas their existence and functions in allergic diseases have been studied incompletely.

117 The role of IL-33 in the pathogenesis of allergic diseases is incompletely understood.

118 Most allergic diseases, such as asthma, rhinitis, food allerg

119 be used to report the seasonal variations of allergic diseases.

120 responsible for the increasing prevalence of allergic diseases.

121 ne disorders, cancer, and cardiovascular and allergic diseases.

122 garding the relevance of anti-glycan IgE for allergic diseases.

123 reventative, and participatory approaches in allergic diseases.

124 reatment of infections and cancer as well as allergic diseases.

125 tic purposes or therapeutic interventions of allergic diseases.

126 target for EoE and related eosinophilic and allergic diseases.

127 e PUFAs may be important in the aetiology of allergic diseases.

128 associated immune responses in patients with allergic diseases.

129 to be used for the prevention of asthma and allergic diseases.

130 hypothesized to influence the development of allergic diseases; however, few prospective studies have

131 Important allergic disorder associations will be missed without su

132 elopmental contribution to the risk of later allergic disorders and suggest that involvement of epige

133 uction and treatment of autoimmune diseases, allergic disorders, and graft rejection by depleting und

134 iated with risk of childhood asthma or other allergic disorders.

135 to an even broader list of hypersensitivity/allergic disorders.

136 for the design of novel immunotherapies for allergic disorders.

137 correlates with a reduced risk of atopy and allergic disorders; however, limited data are available

138 ty by targeting the surface-bound IgE of the allergic effector cells via low-affinity anti-human IgE

139 specific suppression of ongoing experimental allergic encephalomyelitis (an MS animal model), and the

140 there are differences in rates of immediate allergic events between classes of gadolinium-based cont

141 ation of SPT and BAT correctly distinguished allergic from tolerant patients for walnut (87%), pecan

142 IA) patients with suspected MA, and non-meat-allergic healthy control individuals (HC), were analyzed

143 Our data indicate that 9cRA modulates the allergic immune response by reducing the IgE response bu

144 Thus 9cRA can modulate the allergic immune response toward a non-IgE condition.

145 was highly successful in rapidly suppressing allergic immune responses and achieving safe dietary rei

146 ely that recurrence of the T-cell drivers of allergic immunity abrogated the potential for durable to

147 d protein targets of T cell responses in HDM-allergic individuals, and investigate their correlation

148 demonstrated during rhinovirus infection in allergic individuals.

149 IgE-mediated peanut allergy against 148 non-allergic infants (all 1 year old).

150 nexin V positivity, P < .005), and less lung allergic inflammation (number of lung eosinophils, P < .

151 he airways is involved in the development of allergic inflammation and airway hyperresponsiveness (AH

152 tokines in the initiation and maintenance of allergic inflammation and the atopic march.

153 nance of persistent TH2 cells and potentiate allergic inflammation are not well understood.

154 the importance of neuro-immune crosstalk in allergic inflammation at mucosal surfaces.

155 rus infection and the exacerbation of type-2 allergic inflammation in humans.

156 dust mite- and Aspergillus fumigatus-induced allergic inflammation in murine models.

157 ults suggest that urban PM2.5 may exacerbate allergic inflammation in the murine lung via a TLR2/TLR4

158 or allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment

159 the regulation of dendritic cell (DC)-driven allergic inflammation remain elusive.

160 oduction, peri-vascular, peri-bronchial, and allergic inflammation that was unresponsive to inhaled c

161 Interestingly, although the DEP-enhanced allergic inflammation was marginally reduced in ILC2-def

162 ays inflammation in ROCK2-insufficient mice, allergic inflammation was not different in ROCK2(CD)(4Cr

163 critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (

164 cells of the innate immune system linked to allergic inflammation.

165 dysregulation manifesting as autoimmunity or allergic inflammation.

166 ient subpopulation with increased esophageal allergic inflammation.

167 described to regulate adaptive responses in allergic inflammation.

168 way to better treatment based on disrupting allergic inflammatory and type 2 cytokine-mediated respo

169 bility of Lactococcus lactis G121 to prevent allergic inflammatory reactions.

170 to the pathogenesis of Th2-driven asthma and allergic lung diseases.

171 Anaphylaxis and allergic lung inflammation were restored in ADAM10(DC)(-

172 associated with IRF4 and NFAT1 expression in allergic lung inflammation.

173 llergy (CMA) have an increased risk of other allergic manifestations (AMs).

174 ed R gnavus was observed before the onset of allergic manifestations, and was associated with respira

175 The children with allergic manifestations, particularly asthma, during chi

176 l n=533 (n=203 food-allergic, n=330 non-food-allergic), mean age 2.5 years, with food allergy defined

177 henotypes, reduced serum immunoglobulins and allergic mediators, lower mast cells and eosinophil coun

178 cient in de novo generation of Treg cells in allergic mice.

179 f S. aureus carriage and SE sensitization on allergic multimorbidity and allergic sensitization is un

180 eus carriage and severe allergic disease and allergic multimorbidity.

181 paediatric cohorts, total n=533 (n=203 food-allergic, n=330 non-food-allergic), mean age 2.5 years,

182 (46%) from 209 patients had anaphylaxis and allergic or hypersensitivity comorbidities description.

183 From all 2318 files related to allergic or hypersensitivity conditions, 673 had some of

184 d as the occurrence of respiratory, cardiac, allergic, or neurological complications requiring immedi

185 ing with a dog in the first year of life and allergic outcomes vary within subgroups selected a prior

186 compared with its native form, using various allergic parameters in Balb/c mice.

187 ine release in blood basophils obtained from allergic patients (n=11) and nonallergic donors (n=5).

188 rikingly, similar responses were observed in allergic patients and beekeepers after venom exposure.

189 C3 frequency was reduced in tonsil tissue of allergic patients and in peripheral blood of allergic as

190 correlations of r = -0.871 for grass pollen-allergic patients and r = -0.795 for birch pollen-allerg

191 increased IFN-gamma production in B cells of allergic patients during the build-up phase of allergen-

192 lly allergen-reactive PBMC from birch pollen-allergic patients together with birch pollen extract and

193 D86 on monocyte-derived dendritic cells from allergic patients was analyzed by using flow cytometry.

194 ysicians who can deliver optimal care to the allergic patients, the EAACI Specialty Committee propose

195 nt or reverse the process of barrier loss in allergic patients.

196 esulted in a protein unable to bind IgE from allergic patients.

197 ifood oral immunotherapy benefited multifood allergic patients.

198 gic patients and r = -0.795 for birch pollen-allergic patients.

199 cause severe anaphylaxis in untreated venom-allergic patients.

200 The findings were most evident for allergic phenotypes of asthma and rhinitis.

201 y of glycated protein was observed as lesser allergic phenotypes, reduced serum immunoglobulins and a

202 the time course of the early (EAR) and late allergic reaction (LAR).

203 om allergy is a potentially life-threatening allergic reaction following a honeybee, vespid, or ant s

204 t mediator of protective immunity as well as allergic reaction, but how high affinity IgE antibodies

205 s, shrimps are the most predominant cause of allergic reactions and thus more extensively studied.

206 is consistent with the observation that most allergic reactions are in connection with roasted peanut

207 scribed the frequencies and risk factors for allergic reactions caused by accidental allergen ingesti

208 ll differences in sensitization and reported allergic reactions for select tree nuts, with levels bei

209 We conducted a systematic review of (1) allergic reactions to botulinum antitoxin and (2) the pr

210 venom-related anaphylaxis also occur during allergic reactions to food in 22 patients with peanut al

211 rved in school or brought from home reported allergic reactions to nuts.

212 is is the most severe and frightening of the allergic reactions, placing patients at high risk and de

213 -food allergies often associated with severe allergic reactions.

214 We report a novel approach to block allergic reactivity by targeting the surface-bound IgE o

215 ssment of safety, pharmacodynamics and nasal allergic reactivity following repeated weekly intranasal

216 parasites is associated with amelioration of allergic reactivity, but mechanistic insights into this

217 esis that pulmonary eosinophilia linked with allergic respiratory disease is able to promote antivira

218 mmunotherapy, the aetiological treatment for allergic respiratory diseases, has demonstrated to be an

219 Shedding light on the crosstalk between allergic response and cancer is paving the way for new a

220 and basophils, with release of agents of the allergic response, ensues when multivalent antigens bind

221 zed mice resulted in a dramatic reduction of allergic response, indicating the role of B cells in amp

222 ntibodies were the effector molecules of the allergic response.

223 tes mast cells and basophils, initiating the allergic response.

224 importance of B cells in maintenance of the allergic response.

225 port that IL-15(-/-) mice developed enhanced allergic responses in an OVA-induced model of AAD.

226 exert strongly suppressive functions toward allergic responses induced by naive and in vivo-primed h

227 ultimately mediates said innate and adaptive allergic responses is poorly understood.

228 ard infusion-related adverse effects such as allergic responses.

229 C2s) can also contribute to orchestration of allergic responses.

230 Diagnoses of current allergic rhinitis (AR) related to mite allergy and asthm

231 allergen challenge (NAC) is a human model of allergic rhinitis (AR) that delivers standardized allerg

232 Allergic rhinitis (AR) was defined as one or more positi

233 icant impairment of quality of life (QoL) in allergic rhinitis (AR), the degree of impairment in QoL

234 Despite the socioeconomic importance of allergic rhinitis (AR), very few prospective studies hav

235 on with patients suffering from IgE-mediated allergic rhinitis (n=10) and healthy controls (n=10).

236 Participants with allergic rhinitis (n=42) were randomized to receive eigh

237 Perennial allergic rhinitis (PAR) represents a global and public h

238 is effective in patients with IgE-dependent allergic rhinitis and asthma.

239 UFAs were associated with increased risks of allergic rhinitis and eczema up to 18 years, and sensiti

240 technologies in rhinitis control, the ARIA (Allergic Rhinitis and its Impact on Asthma) score rangin

241 , while the effect is mainly confined to non-allergic rhinitis and more pronounced in adolescents tha

242 Mobile technology has been used to appraise allergic rhinitis control, but more data are needed.

243 ndation 1: For initial treatment of seasonal allergic rhinitis in persons aged 12 years or older, rou

244 For treatment of moderate to severe seasonal allergic rhinitis in persons aged 12 years or older, the

245 Allergic rhinitis is diagnosed by history and examinatio

246 In PBMCs of allergic rhinitis participants, 42 sites showed signific

247 Data on asthma, eczema, and allergic rhinitis were captured by validated Internation

248 The risk factors for asthma (e.g., allergic rhinitis) that were identified either by NLP or

249 o allergic conditions (food allergy, asthma, allergic rhinitis, allergic conjunctivitis, and eosinoph

250 ified from four recent systematic reviews on allergic rhinitis, asthma, food allergy and venom allerg

251 henotype was only positively associated with allergic rhinitis.

252 e and reflects the real-life epidemiology of allergic rhinitis.

253 ntradermal immunotherapy in the treatment of allergic rhinitis.

254 notherapy targets the immunological cause of allergic rhinoconjunctivitis and allergic asthma and has

255 en children and adults treated with SLIT for allergic rhinoconjunctivitis.

256 loped to treat grass pollen-induced seasonal allergic rhinoconjunctivitis.

257 spergillus flavus which is a common cause of allergic rhinosinusitis, postoperative aspergillosis and

258 that influence the development of childhood allergic sensitization and atopic diseases.

259 years of life have been linked with risk of allergic sensitization and disease.

260 imuli are associated with the development of allergic sensitization and recurrent wheeze.

261 ith FcepsilonRI is primarily responsible for allergic sensitization and the inflammatory response, wh

262 Atopic dermatitis and allergic sensitization had significant interactions on b

263 et v 1-specific CD4(+) T cells and prevented allergic sensitization in a mouse allergy model.

264 We compared allergic sensitization in patients with food allergy or

265 Elevated hs-CRP is associated with allergic sensitization in school-aged children suggestin

266 The development of specific allergic sensitization in the skin of those patients fol

267 ve interaction between atopic dermatitis and allergic sensitization in their effects on food allergy

268 hanism underlying clinical observations that allergic sensitization is associated with increased susc

269 sensitization on allergic multimorbidity and allergic sensitization is unclear.

270 eak overall increased risk of eczema but not allergic sensitization or physician-diagnosed allergy at

271 n-diagnosed asthma or recurrent wheezing and allergic sensitization to food or environmental antigens

272 nd the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple foods.

273 ss, lung resistance, and TH2 responses after allergic sensitization to ovalbumin.

274 Atopic dermatitis without allergic sensitization was not associated with an increa

275 atures with the exception of some markers of allergic sensitization, indicating a need to develop bet

276 e causal effect of BMI on asthma, hay fever, allergic sensitization, serum total immunoglobulin E (Ig

277 y through modulating susceptibility to early allergic sensitization, upper respiratory tract coloniza

278 pe of enhanced eosinophilic inflammation and allergic sensitization.

279 gands, but not proteases, induced TNF during allergic sensitization.

280 Multiple allergic sensitizations are common in persistent childho

281 Allergic side effects during E-OIT were common but all w

282 ) in the high-dose group; only one (an acute allergic skin reaction in the low-dose group) was assess

283 particularly the assessment of the patient's allergic status.

284 Analyses in 21 additional peanut allergic subjects replicate major findings.

285 controlled pilot trial in which birch pollen allergic subjects were challenged intranasally with omal

286 is also reactive with IgE from sera of maize-allergic subjects.

287 is the dose that elicits a reaction in 5% of allergic subjects.

288 basophil degranulation, and Cyp c 1-induced allergic symptoms in the mouse model.

289 can play an important role in development of allergic symptoms, such as those associated with pollen-

290 ces the release of soluble mediators causing allergic symptoms.

291 In addition, neonatal hyperoxia promoted allergic TH responses to house dust mite exposure.

292 Forty-two were allergic to cashew, and 19 were tolerant.

293 ontrolled immunotherapy studies, 33 patients allergic to grass pollen and 94 to birch pollen complete

294 Thirteen patients allergic to one kind of PPI could tolerate other structu

295 e sensitized to 5-6 tree-nuts, over 50% were allergic to only 1-2 tree-nuts.

296 e of IgE sensitization to PHO and SUX among 'allergics' were monitored.

297 ere significantly associated (p < 0.05) with allergic wheeze (18 positive, 1 negative) and 21 pestici

298 tive, 1 negative) and 21 pesticides with non-allergic wheeze (19 positive, 2 negative); 11 pesticides

299 rently used pesticides with allergic and non-allergic wheeze among male farmers.

300 a label of penicillin allergy (PenA) are not allergic when comprehensively investigated.