ライフサイエンスコーパス: allergic disease

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

2 into practice in the clinical management of allergic disease.

3 s with at least 1 first-degree relative with allergic disease.

4 As) are hypothesized to modulate the risk of allergic disease.

5 IgE(+) B cells during PC differentiation and allergic disease.

6 clinical practice associated with paediatric allergic disease.

7 y and also on the prevalence and severity of allergic disease.

8 s, such as probiotics, for the prevention of allergic disease.

9 ceptors FcRI and CD23 play a central role in allergic disease.

10 missions, has increased at a similar rate to allergic disease.

11 tween alcohol consumption and IgE levels and allergic disease.

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

13 to the long-term effects of breastfeeding on allergic disease.

14 he type 2 immune responses that characterize allergic disease.

15 and in children with self-reported manifest allergic disease.

16 ds (FAs) have been associated with childhood allergic disease.

17 th high IgE levels but not with high risk of allergic disease.

18 pathway is a potential therapeutic target in allergic disease.

19 resent a new therapeutic avenue for managing allergic disease.

20 th high IgE levels but not with high risk of allergic disease.

21 ed between age at the first dose of DTaP and allergic disease.

22 ecular programmes associated with health and allergic disease.

23 t immunizations may affect susceptibility to allergic disease.

24 the maternal diet and outcomes of childhood allergic disease.

25 ccination has been linked to reduced risk of allergic disease.

26 incidence of immunoglobulin E (IgE)-mediated allergic disease.

27 ride, influences the onset of autoimmune and allergic disease.

28 of house dust mite (HDM)-induced respiratory allergic disease.

29 0.013) and were more likely to have comorbid allergic disease.

30 ong-term curative potential in patients with allergic disease.

31 tween alcohol consumption and IgE levels and allergic disease.

32 host housekeeping functions and can suppress allergic disease.

33 fh cells and IL-21 in human and experimental allergic disease.

34 ed trials (RCTs) on outcomes of IgE-mediated allergic disease.

35 effects on susceptibility to infections and allergic disease.

36 es an immune environment more susceptible to allergic disease.

37 ues to possible therapeutic opportunities in allergic disease.

38 ociated with postnatal B-cell maturation and allergic disease.

39 children and their mothers at risk of having allergic disease.

40 lls, with special emphasis on their roles in allergic disease.

41 rway hyperresponsiveness, and no concomitant allergic disease.

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

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

44 uents and proteases, causing or exacerbating allergic disease.

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

46 ct against egg allergy in infants at risk of allergic disease.

47 hildhood may contribute to the prevention of allergic disease.

48 be exploited for therapeutic intervention in allergic disease.

49 is a central feature in the pathogenesis of allergic disease.

50 care and other products, are associated with allergic disease.

51 lammation, including symptoms of "classical" allergic disease.

52 appears to pre-date atopy and development of allergic disease.

53 sponse and contribute to the exacerbation of allergic diseases.

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

55 novel therapeutic approach for IgE-mediated allergic diseases.

56 associated immune responses in patients with allergic diseases.

57 derate agreement, but have a similar AUC for allergic diseases.

58 little is known about their association with allergic diseases.

59 btypes are more at risk for developing other allergic diseases.

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

61 iologics used for diagnosis and treatment of allergic diseases.

62 axis presents new potential drug targets for allergic diseases.

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

64 ole of IL-27 for the control of Th2-mediated allergic diseases.

65 approach for mast cell-specific treatment of allergic diseases.

66 ective function, type 2 immunity also drives allergic diseases.

67 in many clinical trials on asthma and other allergic diseases.

68 ent strategies in patients with inflammatory/allergic diseases.

69 the childhood phenotype and including other allergic diseases.

70 sociated with the persistence or severity of allergic diseases.

71 rately identifying genetic associations with allergic diseases.

72 f PI3K p110delta might be useful in treating allergic diseases.

73 free and self-administered immunotherapy for allergic diseases.

74 for patients with respiratory, IgE-mediated allergic diseases.

75 is a standard route for the immunotherapy of allergic diseases.

76 responsible for the increasing prevalence of allergic diseases.

77 rgens that induce allergic sensitization and allergic diseases.

78 ic diseases, and 7.5 (95% CI, 6.2-9.0) for 3 allergic diseases.

79 e of the epithelial barrier in patients with allergic diseases.

80 play an important role in the development of allergic diseases.

81 urrently in development for the treatment of allergic diseases.

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

83 reactions and forestall the rising trend of allergic diseases.

84 nisms of allergy as well as to better manage allergic diseases.

85 e understanding, diagnosis, and treatment of allergic diseases.

86 play a crucial role in the immunogenicity of allergic diseases.

87 ized for their pathogenic role in asthma and allergic diseases.

88 with reduced risk of food allergy and other allergic diseases.

89 dander and common pollens relevant to human allergic diseases.

90 ating patients' IgG glycosylation profile in allergic diseases.

91 and to test the same variants against other allergic diseases.

92 significant findings also against the other allergic diseases.

93 promising therapeutic strategy for managing allergic diseases.

94 pregnancy or early infancy for prevention of allergic diseases.

95 Th2 cytokine and IL-31 signaling involved in allergic diseases.

96 he development of several biologics to treat allergic diseases.

97 boxane, or serotonin) in the pathogenesis of allergic diseases.

98 y (IT) represents an effective treatment for allergic diseases.

99 nsitization pattern and its association with allergic diseases.

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

101 reventative, and participatory approaches in allergic diseases.

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

103 tween atopic dermatitis phenotypes and other allergic diseases.

104 of immune tolerance, becomes insufficient in allergic diseases.

105 17-producing T cells have important roles in allergic diseases.

106 lls that may be harnessed for the control of allergic diseases.

107 rise as a new target for the manipulation of allergic diseases.

108 re common among some congenital and acquired allergic diseases.

109 IgE is a therapeutic target in patients with allergic diseases.

110 fatty acids influence the risk of childhood allergic diseases.

111 entially more efficient way of treatment for allergic diseases.

112 tic purposes or therapeutic interventions of allergic diseases.

113 target for EoE and related eosinophilic and allergic diseases.

114 enterotoxins (SEs) have been associated with allergic diseases.

115 in the maintenance of immune homeostasis in allergic diseases.

116 vironmental allergens and protecting against allergic diseases.

117 matic reviews on epidemiological research on allergic diseases.

118 rgic disease was 2.3 (95% CI, 2.2-2.5) for 1 allergic disease, 3.9 (95% CI, 3.5-4.4) for 2 allergic d

119 t epigenetic inheritance induced by parental allergic disease activity.

120 Allergic disease affects 30% to 40% of the world's popul

121 Allergic disease affects millions.

122 stigated associations between IgE levels and allergic disease (allergic asthma, rhinitis, and eczema)

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

124 patients with one or more of 11 potentially allergic diseases (anaphylaxis, angioedema, asthma, conj

125 t has been implicated in the pathogenesis of allergic disease and airway viral responses.

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

127 l S. aureus carriage and SE sensitization to allergic disease and allergic sensitization.

128 evolutionary and physiologic foundations of allergic disease and defining what about our modern envi

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

130 ear in infants who are at hereditary risk of allergic disease and had no eczema symptoms at study ent

131 (DC) therapy is effective in mouse models of allergic disease and has been shown to work with TH2 cel

132 ivated Th2 cells from mice with experimental allergic disease and in Th2 polarization cultures.

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

134 imited data on possible long-term effects on allergic disease and lung function.

135 The prevalence of allergic diseases and asthma has dramatically increased

136 play an important role in the development of allergic diseases and asthma.

137 play important roles in the pathogenesis of allergic diseases and asthma.

138 on-approved drugs, may be useful in treating allergic diseases and asthma.

139 (AIT) is an effective treatment strategy for allergic diseases and has been used for more than 100 ye

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

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

142 is spp. seropositivity and associations with allergic diseases and sensitization, in 2 generations in

143 cterizing the pathophysiology of respiratory allergic diseases and the pharmacological properties of

144 can contribute to pathology in patients with allergic diseases and to fatal anaphylaxis.

145 advantaged urban children have high rates of allergic diseases and wheezing, which are diseases assoc

146 ergen-specific IgE is the causative agent of allergic disease, and antibodies contribute to SIT, but

147 d associations between n-3 and n-6 PUFAs and allergic disease, and the magnitude of this effect varie

148 llergic disease, 3.9 (95% CI, 3.5-4.4) for 2 allergic diseases, and 7.5 (95% CI, 6.2-9.0) for 3 aller

149 : 1.92, 8.33)), family history of non-ocular allergic diseases (AOR = 3.57(95 % CI: 1.39, 9.09).

150 I: 4.16, 20.0)), child history of non-ocular allergic diseases (AOR = 4.0 (95 % CI: 1.92, 8.33)), fam

151 nical trials of drug repurposing efficacy in allergic disease are reviewed.

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

153 logical data on infant feeding practices and allergic diseases are controversial.

154 Allergic diseases are driven by activation of mast cells

155 fail to maintain tolerance in patients with allergic diseases are not well understood.

156 Allergic diseases are on the increase globally in parall

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

158 th for immunity to helminth infection and in allergic disease, are currently poorly understood.

159 nts; 76% of LEAP participants had at least 1 allergic disease at 60 months of age.

160 years were associated with a reduced risk of allergic disease at age 16 years.

161 ion enhances subsequent development of these allergic diseases at age 3 years.

162 357; 2010-2015) studied the complex links of allergic diseases at the clinical and mechanistic levels

163 ment containing IL-4 and TGF-beta, promoting allergic disease, autoimmunity, and resistance to pathog

164 reciation of heterogeneity within asthma and allergic diseases based primarily on recent cluster anal

165 Experimental models of allergic disease, basic mechanisms, clinical mechanisms

166 Experimental models of allergic disease, basic mechanisms, clinical mechanisms,

167 IgE-associated allergic diseases belong to the most common inflammatory

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

169 ption is associated with high IgE levels and allergic disease both observationally and genetically us

170 classification proposal of hypersensitivity/allergic diseases built by crowdsourcing the Allergy Aca

171 ong-lasting clinical benefit to IgE-mediated allergic diseases, but a fewer than 5% of patients choos

172 We identified 352 Read codes for these allergic diseases, but only 36 codes (10%) were used in

173 establish tolerance in patients with chronic allergic diseases by promoting Treg cell stability and f

174 a promising therapeutic approach in treating allergic diseases by suppressing ILC2 function.

175 ing maternal n-3 LC-PUFA intake to childhood allergic disease cannot unequivocally be confirmed or re

176 Allergic diseases caused by fungi are common.

177 nstrated that helminth infections ameliorate allergic diseases, clinical trials in humans have not sh

178 seline for future directions to intervene in allergic disease development, progression, or both.

179 Histamine, a major mediator in allergic diseases, differentially regulates the polarizi

180 tions in the development of asthma and other allergic diseases during childhood.

181 maternal n-3 LC-PUFA intake and outcomes of allergic disease (eczema, rhino-conjunctivitis, asthma)

182 The pathogenesis of allergic diseases entails an ineffective tolerogenic imm

183 introduction of peanut on the development of allergic disease, food sensitization, and aeroallergen s

184 asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located i

185 1180 in IL1RL1 was associated with any other allergic disease (for hay fever, OR 0.64, 95% CI 0.53-0.

186 ity of biologic agents for the management of allergic diseases has been facilitated by recent advance

187 Atopy, an endotype underlying allergic diseases, has a substantial genetic component.

188 Immunotherapy, commonly used to treat other allergic diseases, has shown promise as a disease-modify

189 he associations between breast milk PUFA and allergic disease have not previously been systematically

190 c causes for severe manifestations of common allergic diseases have been identified.

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

192 functionality of Treg cells in patients with allergic diseases: how Treg cells are essential in promo

193 have been hypothesized to affect the risk of allergic disease; however, it is unclear whether these a

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

195 triclosan and paraben exposure and childhood allergic disease in a prospective longitudinal study.

196 ic, and environmental status, and history of allergic disease in affected children and their family m

197 iations between early food sensitization and allergic disease in birth cohorts.

198 seeks to reduce the expression of end-organ allergic disease in children with established FA.

199 responses influence the risk of IgE-mediated allergic disease in humans.

200 cooking, child dust exposure, and non-ocular allergic disease in the child or their family were stati

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

202 ny or exclusive) had no effect on asthma and allergic disease in the IoW cohort.

203 irth of a child both pose risks to childhood allergic disease in the offspring, especially for asthma

204 ing these nutrients to prevent or ameliorate allergic disease in their offspring.

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

206 sIgE, and to compare their association with allergic diseases in 10-year-old children.

207 Allergic diseases in animals are increasingly gaining im

208 on between serum IgG glycome composition and allergic diseases in children.

209 ight be associated with an increased risk of allergic diseases in offspring.

210 n challenge-confirmed food allergy and other allergic diseases in preschool-aged children remain spar

211 a role in the development and progression of allergic disease, in particular allergic respiratory dis

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

213 nnection between air pollution and increased allergic disease incidence is DNA methylation, an epigen

214 ions for immune system modulation and asthma/allergic disease incidence.

215 om these studies that may modify the risk of allergic disease include microbial exposures including p

216 y eQTLs located in established risk loci for allergic disease, including 6 genes not previously impli

217 eatment completely inhibited all features of allergic disease, including AHR and eosinophil infiltrat

218 ated to explain the increasing prevalence of allergic disease, including asthma.

219 holds that resistance to the development of allergic diseases, including allergic rhinoconjunctiviti

220 il numbers are associated with infection and allergic diseases, including asthma, but there is also e

221 rin (BCG) vaccination may reduce the risk of allergic diseases, including atopic dermatitis.

222 gation period, 20 children (45.5%) developed allergic diseases, including respiratory (allergic rhini

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

224 The pathology of allergic diseases involves type 2 immune cells, such as

225 ophagitis (EoE), an emerging tissue-specific allergic disease, involves dysregulated gene expression

226 imary step in food allergies, leads to other allergic disease is a controversial but important issue.

227 ence for breastfeeding to prevent asthma and allergic disease is conflicting.

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

229 hol consumption leads to high IgE levels and allergic disease is unclear.

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

231 Clearly, the best clinical outcome for allergic diseases is not to get them in the first place.

232 ation of precision medicine in management of allergic diseases is of utmost importance.

233 autoimmune diseases; however, their role in allergic diseases is poorly understood.

234 n exposure to the relevant allergen and the "allergic" disease is not clear.

235 role for AD as an entry point for subsequent allergic disease, is a phenomenon known as the "atopic m

236 diseases and the incidence of autoimmune and allergic diseases led to the so-called 'hygiene hypothes

237 lity of barrier dysfunction in initiation of allergic disease, many important questions remain to be

238 Having an allergic disease may have health implications beyond tho

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

240 elderly, as indicated by the presence of an allergic disease, might therefore be associated with dif

241 Bedroom allergen exposures contribute to allergic disease morbidity because people spend consider

242 t these basic mechanisms take place in human allergic disease, notably with regard to different clini

243 Eosinophilic esophagitis (EoE) is an allergic disease of increasing worldwide incidence.

244 Asthma and allergic diseases of childhood are highly heritable, and

245 but have yet to develop severe forms of the allergic disease, or who are susceptible to allergy deve

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

247 lights some of the advances in mechanisms of allergic disease, particularly anaphylaxis, including fo

248 eported, which implicate 132 nearby genes in allergic disease pathophysiology.

249 ciation study (GWAS; n = 360,838) of a broad allergic disease phenotype that considers the presence o

250 Allergic disease phenotypes were defined by using questi

251 Having an allergic disease (pollinosis) at an older age may be ind

252 Allergic disease prevalence has increased significantly

253 ease maternal n-3 PUFA intake may not aid in allergic disease prevention.

254 d associations between antibiotic orders and allergic diseases, providing evidence of a potentially m

255 type 2/Th2 cytokines implicated in numerous allergic diseases ranging from asthma to atopic dermatit

256 ntion guidelines for infants at high risk of allergic disease recommend hydrolysed formula if formula

257 We now understand that in patients with allergic disease, regardless of tissue location, the hom

258 lie T helper type 2 cell-driven (Th2-driven) allergic diseases remain unclear.

259 exposure on the risk of children developing allergic disease remains controversial.

260 al value of BTK inhibition in the context of allergic diseases remains to be determined.

261 es involved in IL-4 responses segregate with allergic disease risk and correlate with IgE levels in h

262 uration, and may have an important impact on allergic disease risk.

263 ) to identify modifiable factors that affect allergic disease risk.

264 nd does not prevent the development of other allergic disease, sensitization to other food allergens

265 ion was combined with concurrent symptoms of allergic disease, SHS in infancy was associated with an

266 Associations with allergic diseases, skin prick tests and lung function as

267 unclear whether this benefit is allergen and allergic disease specific.

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

269 n-3 LC-PUFA or fish intake and incidence of allergic disease symptoms in the child.

270 Questions on allergic disease symptoms were based on the Internationa

271 atabases using breastfeeding, fatty acid and allergic disease terms.

272 c asthma and rhinitis are two common chronic allergic diseases that affect the lungs and nose, respec

273 esulted in a new classification framework of allergic diseases that could help to improve the underst

274 (SIT) is the most widely used treatment for allergic diseases that directly targets the T helper 2 (

275 lished anti-IgE therapy for the treatment of allergic diseases that prevents IgE from binding to its

276 The increase in allergic diseases that was observed in countries that ha

277 .01 (95% CI, 1.01-1.02) observationally; for allergic disease, the corresponding odds ratios were 0.9

278 elicit a similar immunologic environment as allergic diseases, the association of glycan-specific an

279 For the other allergic diseases, the range was approximately 0.60-0.80

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

281 of principle for a therapeutic approach for allergic disease through ablation of allergic memory TH2

282 ews and meta-analyses on the epidemiology of allergic diseases to assess what has been studied compre

283 e heritability of childhood asthma and other allergic diseases, to attempt to replicate findings from

284 ype 2 inflammation are needed for asthma and allergic disease treatment.

285 possible role as a new therapeutic option in allergic diseases using a humanized mouse model.

286 150 kU/L and compared with subjects without allergic disease was 2.3 (95% CI, 2.2-2.5) for 1 allergi

287 allergen and aeroallergen sensitization and allergic disease was noted across study time points; 76%

288 the ultimate evidence for its role in human allergic diseases was obtained by the efficacy of anti-I

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

290 SHS exposure and symptoms of allergic disease were assessed using repeated parental q

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

292 Infants with a family history of allergic disease were randomized (stratified by centre/m

293 Self-reported allergic diseases were assessed using the Mechanisms of

294 k test, sIgE measurements, and assessment of allergic diseases were performed in children aged 10 yea

295 sensitizations are associated with different allergic diseases which may reflect different underlying

296 identify children at high risk of subsequent allergic disease who may benefit from early life prevent

297 hagitis (EoE) is an emerging tissue-specific allergic disease with an unclear pathogenesis.

298 Parental allergic diseases with first onsets before and after the

299 nd painless technology to treat IgE-mediated allergic diseases with little local skin reaction and a

300 iated with a trend towards increased odds of allergic diseases, with strong associations observed for