ライフサイエンスコーパス: food allergy

1 n as "probable food allergy" or "probable no food allergy".

2 ing a distinct form of food allergy (Class 3 food allergy).

3 sts and immunologists who manage infants for food allergy.

4 e allergens and the presence of IgE-mediated food allergy.

5 ying the sensitization and effector phase of food allergy.

6 suppress murine IgE-mediated anaphylaxis and food allergy.

7 dietary fat might increase susceptibility to food allergy.

8 te to the association between MOD and wheeze/food allergy.

9 understanding of the immunological basis of food allergy.

10 may inform strategies for the prevention of food allergy.

11 including foods, is strongly associated with food allergy.

12 t reproducible genes for an association with food allergy.

13 f novel diagnostic and prognostic methods in food allergy.

14 CD4(+) T cell (T(H)2) states associated with food allergy.

15 munities may be therapeutically relevant for food allergy.

16 s known to modify the microbiome and risk of food allergy.

17 as potential approaches to the treatment of food allergy.

18 f the best way to prevent the development of food allergy.

19 Dog ownership in infancy may prevent food allergy.

20 n microbiota for 8 weeks before induction of food allergy.

21 s more evident among infants with subsequent food allergy.

22 ing together centers focused on the study of food allergy.

23 e association between MOD and wheeze but not food allergy.

24 logical therapies and group interventions in food allergy.

25 s, and dysbiosis precedes the development of food allergy.

26 management and well-being in consumers with food allergy.

27 and environmental factors that contribute to food allergy.

28 olipid in the effector phase of IgE-mediated food allergy.

29 eastfed infants prevented the development of food allergy.

30 n Taiwan, crab is one of the main causes for food allergy.

31 inate those with persistent versus transient food allergy.

32 in immune function among infants at risk of food allergy.

33 p, is largely uninvestigated with respect to food allergy.

34 stakeholders but particularly patients with food allergy.

35 reg at either 6 or 12 months were related to food allergy.

36 ficient to confer enhanced susceptibility to food allergy.

37 the first postnatal year and development of food allergy.

38 ic allergen challenge to induce experimental food allergy.

39 s from immunized mice and from patients with food allergy.

40 he commensal microbiota in susceptibility to food allergy.

41 gy of eczema, allergic rhinitis, asthma, and food allergy.

42 the development and severity of experimental food allergy.

43 d IgE antibody by ingested antigen underlies food allergy.

44 and severity of the disease in our model of food allergy.

45 nificant consequences for the development of food allergy.

46 on of complementary solids may contribute to food allergy.

47 RPINB and C11orf30) that are associated with food allergy.

48 h infants onto a randomized trial to prevent food allergy.

49 patients with asthma, atopic dermatitis, and food allergy.

50 ergic rhinitis, asthma, and challenge-proved food allergy.

51 ing the value of emerging therapies to treat food allergy.

52 l mastocytosis and experimental IgE-mediated food allergy.

53 trials with IL-33 inhibitors are underway in food allergy.

54 lupus erythematosus to atopic dermatitis and food allergy.

55 nsidered as a strategy for the prevention of food allergy.

56 events mediating the regeneration of IgE in food allergy.

57 thma, allergic and nonallergic rhinitis, and food allergy.

58 naling on MMC9s in experimental IgE-mediated food allergy.

59 and MMC9-dependent experimental IgE-mediated food allergy.

60 n of related allergic diseases, particularly food allergy.

61 and biomarkers of allergic disorders such as food allergy.

62 a form of non-IgE-mediated gastrointestinal food allergy.

63 ll activation in the intestine in a model of food allergy.

64 lex role monocytes play in disorders such as food allergies.

65 imited, and particularly so for IgE-mediated food allergies.

66 food industry for the benefit of people with food allergies.

67 udy the relationship between respiratory and food allergies.

68 py (EPIT) is a promising method for treating food allergies.

69 ew therapies for the treatment of persistent food allergies.

70 for patients with concurrent PN/TN and other food allergies.

71 ng number of people suffer from IgE-mediated food allergies.

72 ology of B cells in relation to IgE-mediated food allergies.

73 represent a chronic condition in humans with food allergies.

74 feeding in all infants, including those with food allergies.

75 topic eczema (6[5%] of 118 vs 3[2%] of 137), food allergy (4[3%] of 124 vs 2[1%] of 154), wheeze (39[

76 Bet v 1-mediated birch pollen and associated food allergies, a single wild-type allergen does not pro

77 Food allergy accounted for 71% of the symptoms, with whe

78 reduction in the odds of infants developing food allergy (adjusted odds ratio (aOR) 0.10 (confidence

79 erval: 1.31, 4.66), and an increased risk of food allergy, adjusting for maternal atopy, prepregnancy

80 epresentatives, researchers, regulators, and food allergy advocates came together to discuss OIT and

81 Food allergy affects a small but important number of chi

82 Food allergy affects a small but significant number of c

83 0.5% (95% CI, 0.1% to 1.8%) of children had food allergy, all to egg.

84 Evidence on food allergies, allergic rhinitis, and atopic dermatitis

85 y of human milk by bottle versus breast with food allergies, allergic rhinitis, atopic dermatitis, an

86 skin barrier impairment, atopic dermatitis, food allergy, allergic asthma, and allergic rhinitis, it

87 Allergic disorders include food allergy, allergic rhinitis, and certain forms of as

88 unotherapy, asthma, dermatological diseases, food allergies, anaphylaxis, insect venom, and drug alle

89 ditions such as inflammatory bowel diseases, food allergies and invasive gastrointestinal infections(

90 ine mast cells and for the manifestations of food allergy and anaphylaxis.

91 Allergies, including asthma, food allergy and atopic dermatitis, are increasing in pr

92 e (after 4 mo) does not increase the risk of food allergy and atopic dermatitis/eczema but may preven

93 Food allergy and autoantibodies occurred concomitantly i

94 In contrast to respiratory allergy, food allergy and autoantibody formation occurred togethe

95 cant relationships were demonstrated between food allergy and caesarean delivery, infections or antib

96 ergenic epitopes is a sensitive biomarker of food allergy and can be used to predict allergy severity

97 thology in non-IgE mediated gastrointestinal food allergy and Crohn's disease, we tested whether ther

98 e gastrointestinal microbiota contributes to food allergy and discuss our vision for the future of th

99 oped for adults and parents of children with food allergy and distributed across Germany, Ireland, Ne

100 dividuals at risk of developing IgE-mediated food allergy and hence provide a window for therapeutic

101 Further understanding of the mechanisms of food allergy and identification of biomarkers to disting

102 pollen immunotherapy in birch pollen-related food allergy and indicate a dominant protective role of

103 erapy has shown promise for the treatment of food allergy and is currently being evaluated in clinica

104 have an unexpected helper role in promoting food allergy and may represent a target for drug develop

105 mentary solids, excluding milk products, and food allergy and sensitization.

106 al exposures modulate the risk of developing food allergy and some of this may be mediated by the inf

107 in early life to prevent the development of food allergy and summarized the range of opinions amongs

108 AT can also be used to monitor resolution of food allergy and the clinical response to immunomodulato

109 derstanding of the role of the microbiota in food allergy and tolerance, therapeutics aimed at modify

110 alterations as risk factors for experimental food allergy and uncouple a pathogenic role of an HFD-as

111 ctor's diagnoses (asthma, hay fever, eczema, food allergy), and measurement of lung function, FeNO an

112 of allergic diseases like atopic dermatitis, food allergies, and asthma has risen alarmingly over the

113 ood allergies, the pre-graduate education of food allergies, and much more.

114 on can alter the course of childhood asthma, food allergy, and allergic rhinosinusitis.

115 diseases such as allergic rhinitis, asthma, food allergy, and atopic dermatitis has increased dramat

116 for the prevention and management of asthma, food allergy, and atopic dermatitis.

117 ic rhinosinusitis, eosinophilic esophagitis, food allergy, and atopic dermatitis.

118 birth by cesarean section is associated with food allergy, and consumption of fermented milk products

119 predisposition for intestinal inflammation, food allergy, and failure to thrive, often necessitating

120 antibodies are not uniformly associated with food allergy, and intestinal MC load is an important det

121 ode of birth was not associated with risk of food allergy, and there was no evidence that nTreg at ei

122 ted with progression from AD to IgE-mediated food allergy, and white race was associated with progres

123 Food allergies are a major clinical problem and are driv

124 Food allergies are a serious and rising public health co

125 Food allergies are a significant public health issue, an

126 ly, we have a poor understanding of why some food allergies are outgrown and others are not.

127 omising results, existing genetic studies on food allergy are inundated with issues such as inadequat

128 PAL is counterproductive for consumers with food allergies as there is no standardized approach to a

129 tand the pathogenesis and natural history of food allergy, as well as potential approaches to the tre

130 e sought to understand how those living with food allergy assess risk with precautionary allergen lab

131 ed risk of multiple comorbidities, including food allergy, asthma, allergic rhinitis, and mental heal

132 x, birth size), nTreg at each time point and food allergy at 1 year were examined by linear regressio

133 seases, from seasonal hay fever, through the food allergies, atopic eczema, asthma, to anaphylaxis.

134 dated, and new indications were proposed (eg food allergy, atopic dermatitis).

135 nts of CFBs consumed, and the development of food allergy, atopic dermatitis/eczema, asthma, and alle

136 h CF first begins and the risk of developing food allergy, atopic dermatitis/eczema, or childhood ast

137 ery 4-6 months until 3 years of age, as were food allergies beginning at 8 months.

138 With food allergy being a major health problem of increasing

139 whether infants at high risk of developing a food allergy benefited from early introduction.

140 utic approaches in the treatment of not only food allergy but also other immune-mediated diseases.

141 ing solids before 4 months protected against food allergy, but there was evidence for protection agai

142 xP3 regulatory T cells and the prevention of food allergy by OVA exposure through breast milk.

143 ears has demonstrated the significant impact food allergy can have on quality of life and mental heal

144 id not differ between food sensitization and food allergy cases and controls.

145 nophil degranulation, indicating an atypical food allergy characterized by eosinophil activation.

146 lergic reactions, causing a distinct form of food allergy (Class 3 food allergy).

147 vents were mild to moderate, except a severe food allergy considered unrelated to treatment.

148 topic dermatitis, asthma, allergic rhinitis, food allergy, contact allergy, and hand eczema.

149 iFAAM consensus guidance to develop a novel food allergy diagnosis algorithm using available informa

150 Food allergy diagnosis in clinical studies can be challe

151 In the clinical field of food allergies, dietary management towards patients is d

152 eason for this is the possible deficiency of food allergy education during the training courses for r

153 es of registered dietitians, the practice of food allergy education is hardly adequate, and the educa

154 we will investigate the actual situations of food allergy education practiced in the training courses

155 ate of people who strongly feel the need for food allergy education was 49%, and the rate for people

156 He was diagnosed as having immediate-type food allergies (egg, milk and wheat) by oral food challe

157 ence for epithelial dysregulation in asthma, food allergy, eosinophilic esophagitis, and allergic rhi

158 This was implemented by a panel of food allergy experts blind to treatment allocation and O

159 Food allergy (FA) affects an increasing proportion of ch

160 The prevalence of food allergy (FA) among European school children is poor

161 importance of patient history in diagnosing food allergy (FA) and the need for studies investigating

162 Atopic dermatitis (AD) and food allergy (FA) are associated with skin barrier dysfu

163 We show that Treg cells in food allergy (FA) had decreased expression of transformi

164 The steep rise in food allergy (FA) has evoked environmental factors invol

165 Food sensitization and challenge-proved food allergy (FA) have not been compared in urban and ru

166 Food allergy (FA) is a growing health problem worldwide.

167 Food allergy (FA) is a significant public health issue,

168 The prevalence of IgE-mediated food allergy (FA) is increasing worldwide, but the under

169 The role of dysbiosis in food allergy (FA) remains unclear.

170 from AD to other atopic diseases, including food allergy (FA), allergic rhinitis, allergic asthma, a

171 heese consumption on atopic dermatitis (AD), food allergy (FA), allergic rhinitis, asthma, and atopic

172 were to be considered a strategy to prevent food allergy, families of nonwhite ethnicity, those with

173 hort overview of the psychological impact of food allergy, followed by a discussion of the use of pae

174 The food allergy group had a 1.38 times higher rate for cumu

175 The food allergy group showed more than twice the likelihood

176 il the end of January 2020, no treatment for food allergies had been approved by the US Food and Drug

177 Infants that developed food allergy had decreased nTreg at birth, and the labou

178 MS patients with food allergy had more relapses and a higher likelihood o

179 ng increase in the incidence and severity of food allergies has coincided with lifestyle changes in W

180 Food allergies have become a significant heath burden as

181 nological mechanisms that cause IgE-mediated food allergy have been extensively studied.

182 Mechanistic studies in mouse models of food allergy have confirmed that the composition of the

183 udies has demonstrated that individuals with food allergy have distinct gut microbiomes compared to h

184 Mothers of children with food allergy have increased anxiety, which may be influe

185 The genetic determinants of food allergy have not been systematically reviewed.

186 nalysis reviewed laboratory test results and food allergy histories (obtained from medical records) o

187 iewed the literature on the genetic basis of food allergy, identifying areas for further investigatio

188 itions (atopic dermatitis [AD], IgE-mediated food allergy [IgE-FA], asthma, and allergic rhinitis [AR

189 Oral immunotherapy (OIT) for food allergy improves the quality of life (QOL) of child

190 g allergy presents as one of the most common food allergies in children.

191 Short-Term Memory (LSTM) networks to predict food allergies in early life (0-3 years) from subjects'

192 n how breastfeeding can prevent the onset of food allergies in offspring by instructing T reg formati

193 Rates of allergic rhinitis, asthma and other food allergies in PwPA were 50%, 42% and 79%, respective

194 ng generational increase in life-threatening food allergies in Westernized societies(1,2).

195 kg was associated with a 44% greater risk of food allergy in children (odds ratio [OR], 1.44; 95% CI,

196 Food allergy in children can be life-threatening.

197 rithm with high sensitivity for IgE-mediated food allergy in clinical study participants who do not u

198 elivery (CD) increased the risk of wheeze or food allergy in early childhood compared with vaginal de

199 be that the association between S aureus and food allergy in eczematous patients is related to eczema

200 This may be a useful tool for excluding food allergy in future clinical studies where OFC is not

201 of life for primary prevention of eczema and food allergy in high-risk infants (ISRCTN21528841).

202 The generation of IgE-mediated food allergy in humans is silent and only diagnosed upon

203 r understand how commensal bacteria regulate food allergy in humans, we colonized germ-free mice with

204 s effective in preventing the development of food allergy in specific groups of infants at high risk

205 ted with allergic sensitization and clinical food allergy in the first year of life.

206 g pregnancy strongly predicts the absence of food allergy in the offspring.

207 Food allergy in the pig can be associated with esophagit

208 or investigation into multiple mechanisms of food allergy including modification of epithelial metabo

209 Diet-induced obesity and food allergies increase in tandem, but a potential cause

210 ife Questionnaire-Parent Form (FAQLQ-PF) and Food Allergy Independent Measure (FAIM).

211 The prevention of food allergy is a key priority for reducing the burden o

212 Food allergy is a major health problem affecting 5% to 1

213 Food allergy is a major public health concern with avoid

214 Food allergy is associated with a high personal health a

215 2 or increasing Th1 responses can ameliorate food allergy is being enhanced by a more complex model i

216 evement of long-lasting, safe treatments for food allergy is dependent on the understanding of the im

217 Much of the morbidity associated with food allergy is driven by the fear of a severe reaction

218 Food allergy is on the rise, and preventive/therapeutic

219 Food allergy is responsible for considerable morbidity a

220 mportance in Th2 inflammatory responses like food allergy is still unclear.

221 Food allergy is the most common cause of anaphylaxis.

222 Food allergy is usually difficult to diagnose in early l

223 For each food allergy, linear mixed-effects models were built to

224 orders such as asthma, allergic rhinitis and food allergy, mainly by inducing T helper (Th) 2 immune

225 The potentially fatal consequence of food allergies makes managing them costly and anxiety-in

226 induces a tolerogenic immune response in the food allergy model and in human immune cells.

227 d proteins on the immune response in a mouse food allergy model and on human monocyte-derived dendrit

228 ulating Ag-specific IgE using a peanut-based food allergy model in mice.

229 from T cells, basophils, and mast cells in a food allergy model, and deficiency in IL-9 expression re

230 used in vivo and ex vivo endpoints in murine food allergy models, addressing their strengths and limi

231 All patients presented with atopic symptoms (food allergy, n = 13; hay fever, n = 10; asthma, n = 7).

232 Although pollen-related food allergy occurs in all European populations, lipid t

233 roteins (LTPs) are important causes of plant-food allergies often associated with severe allergic rea

234 can imprint susceptibility or resistance to food allergy on the host and have identified a unique po

235 less likely to have a reported diagnosis of food allergy or allergic rhinitis.

236 months vs <4 months was not associated with food allergy (OR 1.01; 95% CI, 0.64-1.60) but was associ

237 months vs <4 months was not associated with food allergy (OR 1.22; 95% CI, 0.76-1.96) but was associ

238 t enough to categorize children as "probable food allergy" or "probable no food allergy".

239 ort studies that have followed children with food allergy over time, but information generated from s

240 evalence of rhinitis (p < .001) and previous food allergy (p < .001), together with a higher proporti

241 ere is an urgent need for a consensus on key food allergy parameters to be applied in future food all

242 nges in gut microbial community structure on food allergy pathogenesis.

243 continue to be developed providing hope for food allergy patients everywhere.

244 We sought to assess food allergy phenotypes in a genetically diverse collect

245 mpact on mast cell-dependent anaphylaxis and food allergy phenotypes in vivo.

246 ndication of patients with ingestion-related food allergy, pollinosis, or oral allergy syndrome conti

247 The Food Allergy Quality of Life Questionnaire-Child Form (F

248 5D-Y, Hospital Anxiety and Depression Scale, Food Allergy Quality of Life Questionnaire-Parent Form (

249 tolerance and the effector pathways driving food allergy remain elusive.

250 IgE-mediated food allergy remains a significant and growing problem a

251 Oral immunotherapy (OIT) for food allergy requires exercise restrictions following th

252 Immunotherapy for food allergy requires prolonged treatment protocols and,

253 Successful prevention of food allergy requires the identification of the factors

254 Food Allergy Research & Education organized the Oral Imm

255 The Consortium for Food Allergy Research (CoFAR) was established by the Nat

256 tion for Applied Scientific Research and the Food Allergy Research and Resource Program at the Univer

257 nisation for Applied Scientific Research and Food Allergy Research and Resource Program to derive ind

258 erived from the union of the major databases Food Allergy Research and Resource Program, Comprehensiv

259 d allergy parameters to be applied in future food allergy research in synergy between both knowledge

260 Consortium for Food Allergy Research investigators previously reported

261 reconstitution-based models of IgE-mediated food allergy revealed an IL-4 signaling-dependent cell-i

262 intrinsic effect on SI MMC9 accumulation and food allergy severity.

263 rom atopic dermatitis, bronchial asthma, and food allergies since childhood.

264 Food allergy status was determined by double-blind place

265 ly improve the health and quality of life of food allergy sufferers.

266 ants living with at least two dogs developed food allergy, suggesting a dose-response relationship (e

267 ucation organized the Oral Immunotherapy for Food Allergy Summit on November 6, 2019, modeled after t

268 unity with long-term effects on IgE-mediated food allergy susceptibility.

269 Food allergy testing is not recommended in the routine e

270 safely suppress IgE-mediated anaphylaxis and food allergy than divalent variants of the same mAbs do.

271 potential risk factor for the development of food allergy, that is, D pteronyssinus allergens in brea

272 nce of lectures or practical trainings about food allergies, the pre-graduate education of food aller

273 groups of infants at high risk of developing food allergy: those sensitized to egg or to any food at

274 c sensitization; nine, wheezing/asthma; six, food allergy; three, allergic rhinitis/conjunctivitis.

275 key role in the development of IgE-mediated food allergies through the production of allergen-specif

276 chieved for the majority of individuals with food allergy through immunotherapy, continued ingestion

277 ation as an important driver of IgE-mediated food allergy through regulation of allergen-specific IgE

278 nt, EIG infants developed significantly less food allergy to 1 or more foods (SIG, 46.7%; EIG, 22.6%;

279 p (EIG) infants developed significantly less food allergy to 1 or more foods than standard introducti

280 ssociated with the induction of IgE-mediated food allergy to red meat.

281 current understanding of T cell functions in food allergy, tolerance, and immunotherapy.

282 The future of food allergy treatment is promising with a number of cli

283 the large number of patients suffering from food allergies, up until the end of January 2020, no tre

284 The prevalence of food allergy was 26% and that of respiratory allergy was

285 IgE-mediated food allergy was determined by food challenge at 1 year.

286 ative preference value set for patients with food allergy was determined using the SF-6Dv2 generic qu

287 Food allergy was diagnosed amongst 6.1% (68/1124) of par

288 Food allergy was induced in young pigs using two protoco

289 tization affects offspring susceptibility to food allergy, we epicutaneously sensitized female mice w

290 cells are seldom considered in IgE mediated food allergy; we show that peanut specific CD8(+) T cell

291 Lectures about food allergies were conducted in 96% of the facilities,

292 Classical food allergies were excluded by negative results from im

293 le sex; (b) Psychological factors-asthma and food allergy were associated with anxiety and depression

294 54 patients aged 12 years old and above with food allergy were recruited in clinic and online.

295 Allergic disease (eczema, atopic eczema, food allergy, wheeze, atopic sensitization) was assessed

296 he immune basis of the natural resolution of food allergy will likely provide critical information fo

297 ies with clinically proven food IgE mediated food allergy with 258 randomly selected mothers.

298 tle genetic research has been carried out in food allergy, with FLG, HLA and IL13 being the most repr

299 than 50% of patients could have nonclassical food allergy, with immediate disruption of the intestina

300 ated with discontinued immunosuppression and food allergy, with odds ratios of 13 (P = 0.01) and 7.1