ライフサイエンスコーパス: allergic

1 ions among children and young adults who are allergic.

2 ained from experiments with murine models of allergic airway and skin inflammation and offer an overv

3 icant role in the pathogenesis of asthma and allergic airway disease (AAD).

4 Augmented IFN-gamma responses in the HDM allergic airway disease model were accompanied by increa

5 uced glycolytic reprogramming contributes to allergic airway disease using a murine house dust mite m

6 nstrated therapeutic effects, on established allergic airway disease, and prevented the development o

7 r management of eosinophilic inflammation in allergic airway disease, including asthma.

8 the effector phase in the ovalbumin-induced allergic airway disease.

9 Eosinophilia is a hallmark of allergic airway inflammation (AAI).

10 cells that mediate IL-9-dependent effects in allergic airway inflammation and anti-tumor immunity.

11 Lastly, ST2 is required for the exacerbated allergic airway inflammation in Bcl6(fl/fl) Foxp3-Cre mi

12 zed settings such as house dust mite-induced allergic airway inflammation, the lack of IRF4 expressio

13 ite (HDM)-induced allergic sensitization and allergic airway inflammation.

14 o determine the role of endothelial miR-1 in allergic airway inflammation.

15 it remains controversial how Notch promotes allergic airway inflammation.

16 he development of acute T(H)2-cell-dependent allergic airway inflammation.

17 ells, including Tfr cells, in the context of allergic airway inflammation.

18 tes eosinophil trafficking in the setting of allergic airway inflammation.

19 a steroid-sensitive, house dust mite-induced allergic airways disease (AAD) model and a steroid-insen

20 plays a crucial role in the pathogenesis of allergic airways disease by increasing IL-1beta-induced

21 e sequence of ovomucoid, in plasma of 38 egg-allergic and 6 atopic children.

22 sponses affect susceptibility to infectious, allergic and autoimmune diseases.

23 immune-mediated diseases such as autoimmune, allergic and chronic inflammatory disorders.

24 IL37 as potential biomarkers to distinguish allergic and irritant contact dermatitis in human skin.

25 Among nickel-specific CD4+ T cells of allergic and non allergic donors, TCRs expressing the al

26 ents by Dunbar on the passive vaccination of allergic animals more than 100 years ago.

27 During that period, pollen allergic as well as non-allergic patients frequently pre

28 in early childhood and their predictors and allergic associations.

29 Allergic asthma (AA) is characterized as a Th2-biased ai

30 rgic rhinoconjunctivitis (PAR) and perennial allergic asthma (PAA) caused by indoor allergens in adul

31 h Factor Binding Proteins (IGFBPs)" route in allergic asthma and the lectin pathway of complement act

32 he importance of PD-1 agonistic treatment in allergic asthma and underscore its therapeutic potential

33 alpha signaling on B cells is deleterious in allergic asthma because it is required for optimal T(H)2

34 Allergic asthma causes substantial morbidity and constit

35 ex and weight gain alters the progression of allergic asthma in mice with females developing airway r

36 Allergic asthma is a chronic disease beginning in childh

37 Allergic asthma is a chronic inflammatory lung disease a

38 Allergic asthma is mediated by Th2 responses to inhaled

39 med/high)CD11c(-/low) phenotypes, similar to allergic asthma models.

40 fferences in the development and severity of allergic asthma observed between men and women of reprod

41 d asthma control was particularly evident in allergic asthma patients and correlated with decreased f

42 l-world setting indicates that patients with allergic asthma who receive AIT are less likely to exper

43 Allergic asthma with high plasma IgE levels is a signifi

44 he three prototype chronic allergic diseases allergic asthma, chronic spontaneous urticaria and atopi

45 -severe rhino-conjunctivitis with or without allergic asthma, the cost-effectiveness of SLIT (tablets

46 educe airway obstruction and inflammation in allergic asthma.

47 LS as a useful biomarker for moderate-severe allergic asthma.

48 LC2(10)s in the development and pathology of allergic asthma.

49 g alveolar macrophages suppressed HDM-driven allergic asthma.

50 active COVID-19 infection in a patient with allergic asthma.(1) There are other emerging reports tha

51 Rhinovirus induces robust T(H)1 responses in allergic asthmatic subjects that may promote disease, ev

52 zing aspergillosis, fungal colonization, and allergic bronchopulmonary aspergillosis.

53 Egg-allergic children had lower esIgA(1) (P = .010) and esIg

54 Food-allergic children not undergoing OIT served as controls.

55 QOL of food-allergic children undergoing OIT improves significantly

56 improve the quality of life for many peanut allergic children.

57 l lesion distribution at the age of 3 years, allergic comorbidities, and disease exacerbation by the

58 ithout FIRE; P < .01) and in those with high allergic comorbidity.

59 ergic march refers to the natural history of allergic conditions during infancy and childhood.

60 us pathogens and source of allergens causing allergic conditions in animals and humans.

61 l interventional designs across the range of allergic conditions is required to strengthen the eviden

62 ies reported effect sizes and no studies for allergic conditions other than asthma met the inclusion

63 i-IgE antibody approved for the treatment of allergic conditions.

64 y adolescents with asthma, less so for other allergic conditions.

65 ed weighted prevalence of reported rhinitis, allergic conjunctivitis and eczema was 43.3%, 39.5% and

66 ing agents in wines may represent a risk for allergic consumers and a source of discomfort for others

67 rgen used in hair dye that is known to cause allergic contact dermatitis (ACD).

68 sident memory T (T(RM)) cells play a role in allergic contact dermatitis (ACD).

69 Nickel-induced allergic contact dermatitis (nACD) remains a major occup

70 y patient risk characteristics, incidence of allergic contact dermatitis, and incidence of wound comp

71 63(-/-) mice show a stronger inflammation in allergic contact dermatitis, indicating a regulatory rol

72 nd NPRA may provide effective treatments for allergic contact dermatitis-associated chronic pruritus.

73 re consistent with previous reports of a low allergic cross-reactivity between PCN and later-generati

74 ght to assess the risk of HL associated with allergic disease (asthma, eczema, and allergic rhinitis)

75 ntrol, psychosocial issues, adolescent-onset allergic disease and female sex; (b) Psychological facto

76 eatment, that modifies the natural course of allergic disease and induces long-term tolerance.

77 phagitis (EoE) is an emerging, chronic, rare allergic disease associated with marked eosinophil accum

78 Known health benefits of SCFAs in allergic disease can, at least in part, be explained by

79 t probiotics are effective for prevention of allergic disease in premature infants remains lacking; a

80 Details of allergic disease outcomes including sensitization, wheez

81 e, we show that the prominent autoimmune and allergic disease risk locus at chromosome 11q13.5(2-7) c

82 iated with increased and some with decreased allergic disease risks over childhood.

83 Subsequent childhood allergic disease was assessed by parent report, clinical

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

85 m-born infants has been suggested to prevent allergic disease, in particular eczema; however, no stud

86 nt in the lung tissue not only in pathology (allergic disease, parasite expulsion) but also during no

87 hat might play a role in human infections or allergic disease.

88 e dose in the prevention of autoimmunity and allergic disease.

89 ly sialylation, as an important regulator of allergic disease.

90 the origin of the various manifestations of allergic disease.

91 al distress increases the risk for childhood allergic disease.

92 iagnosis, management, and prevention of this allergic disease.

93 e Keystone Symposium conference, "Origins of allergic disease: Microbial, epithelial and immune inter

94 developments in the three prototype chronic allergic diseases allergic asthma, chronic spontaneous u

95 as a protective effect on the development of allergic diseases and asthma at the age of 7.

96 baseline to estimate their association with allergic diseases and asthma at the ages of 4 and 7.

97 odies are best known for pathogenic roles in allergic diseases and for protective effector functions

98 s first option in almost 2/3 of all types of allergic diseases and in 90% regarding respiratory aller

99 long implicated in antiparasite immunity and allergic diseases and, more recently, in regulating adip

100 Allergic diseases are more common in Finland than in Est

101 seventh months of life on the prevalence of allergic diseases at school age.

102 In the quantitative analysis, the risk of allergic diseases decreased significantly with increasin

103 The prevalence of allergic diseases differs in urban and rural populations

104 ymptom, suggesting that commonly encountered allergic diseases exist on a spectrum of monogenic and c

105 acilitate clinical decision-making regarding allergic diseases in the context of hematopoietic stem c

106 ve investigated probiotics for prevention of allergic diseases in very preterm infants.

107 ing in the development of oral tolerance and allergic diseases is controversial, which could be relat

108 ggrin gene are a significant risk factor for allergic diseases such as atopic dermatitis, asthma, all

109 between maternal HMO profiles and offspring allergic diseases up to age 18 years.

110 driver of type2/Th2 immune diseases (atopic/allergic diseases).

111 is a type 2 cytokine with important roles in allergic diseases, asthma, and tissue fibrosis.

112 formation was collected on family history of allergic diseases, household size, socioeconomic status,

113 verview of the current research on miRNAs in allergic diseases, including atopic dermatitis, allergic

114 cells that display key effector functions in allergic diseases, such as asthma.

115 ontent in drinking water may protect against allergic diseases.

116 have been widely investigated in asthma and allergic diseases.

117 , and aetiological origins of autoimmune and allergic diseases.

118 evising appropriately targeted therapies for allergic diseases.

119 (Treg) play an important role in preventing allergic diseases.

120 otal cytokines involved in the generation of allergic diseases.

121 ches to the blockade of pathways involved in allergic diseases.

122 arget mast cells during anaphylaxis or other allergic diseases.

123 responsiveness, revealing that patients with allergic disorders have an increased nasal mucosal IFN a

124 actions underlying the early-life origins of allergic disorders, as well as immune mechanisms that mi

125 nd survey its clinical efficacy in different allergic disorders.

126 sents the typical trajectory associated with allergic disorders.

127 an interesting approach for the treatment of allergic disorders.

128 el-specific CD4+ T cells of allergic and non allergic donors, TCRs expressing the alpha-chain segment

129 itional 11 American and 14 Slovakian ragweed allergic donors.

130 allergic inflammation through FcepsilonRI on allergic effector cells, while IgE-ICs were noninflammat

131 lammatory arthritis but also in experimental allergic encephalomyelitis (EAE), a murine model of mult

132 of spectacles or contact lenses, history of allergic eye disease, or pregnancy.

133 tized (NS), sensitizedtolerant (ST), or food allergic (FA) based on skin prick testing and food chall

134 were initially evaluated in the grass pollen-allergic (GPA) group (n = 28) and nonatopic healthy cont

135 Interestingly, within the allergic group, children with higher esIgD had decreased

136 In addition, we also observed that allergic HFD female mice presented a robust lung remodel

137 f immunoglobulin E (IgE) and its key role in allergic hypersensitivity reactions against normally har

138 mained enigmatic, recent evidence shows that allergic immune reactions can help to protect against th

139 llergic-skewing DCs and the initiation of an allergic immune response.

140 , does not lead to durable modulation of the allergic immune response.

141 How T(H)2-mediated allergic immune responses are induced is still under inv

142 previously unknown physiological function of allergic immune responses, IgE antibodies, and MCs in ho

143 tic cells (DCs) of the cDC2 lineage initiate allergic immunity and in the dermis are marked by their

144 roup 2 innate lymphoid cells (ILC2s) mediate allergic immunity but have also recently come into focus

145 ns in indoor air have never been examined in allergic individuals in a controlled exposure setting.Ob

146 nate immune responses of the nasal mucosa in allergic individuals may be important in determining the

147 d immunomodulatory effects in the airways of allergic individuals.

148 d in the diverse T-cell responses in ragweed allergic individuals.

149 ases of the gastrointestinal tract caused by allergic inflammation and gastrointestinal dysfunction.

150 , we aimed to assess the association between allergic inflammation in the lung (asthma), skin (eczema

151 nct biological functions: free IgE initiated allergic inflammation through FcepsilonRI on allergic ef

152 ves as a brake on airway EC responses during allergic inflammation, but is impaired in asthma.

153 when they were obtained from AMs exposed to allergic inflammation-associated cytokines.

154 compounds in reducing Alternaria-stimulated allergic inflammation.

155 l as important future research directions in allergic inflammation.

156 hoid cell (ILC2) activation to induce innate allergic inflammation.

157 4 consecutive days to evaluate innate airway allergic inflammation.

158 atment of eosinophilic esophagitis (EoE), an allergic inflammatory disease of the esophageal mucosa.

159 ed as important factors in the mechanisms of allergic inflammatory diseases.

160 cretion as a mechanism by which AMs restrain allergic inflammatory responses in airway ECs.

161 ding allergen-specific serum IgE production, allergic lung and airway inflammation and airway hyper-r

162 e sought to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the exp

163 In vivo, CO(2) -RWE induced stronger allergic lung inflammation compared to control-RWE, as i

164 e derived from Cpn 60.1, named IRL201104, on allergic lung inflammation induced by ovalbumin (OVA) in

165 abp5(-/-) mice exhibited a severe symptom of allergic lung inflammation.

166 ation of innate lymphoid cell (ILC) 2 during allergic lung inflammation.

167 herapeutic target for treating ILC2-mediated allergic lung inflammation.

168 ial hyperresponsiveness in a murine model of allergic lung inflammation.

169 The allergic march refers to the natural history of allergic

170 features that are associated with the major allergic march trajectories.

171 various important events that exacerbate the allergic microenvironment, including the production of m

172 bial composition of house dust may influence allergic outcomes in adults.

173 s to understand how diet diversity modulates allergic outcomes.

174 ences fetal immune development and postnatal allergic outcomes.

175 rolled trial, 606 newborns with at least one allergic parent received orally a bacterial lysate consi

176 Peanut-allergic patients appear to demonstrate higher absorptio

177 cifically binding the allergens to which the allergic patients are sensitized.

178 ApoA-IV levels were decreased in serum from allergic patients compared to healthy controls.

179 1, 3, 4, 5, 8 and 11) in 20 American ragweed allergic patients determined by FluoroSpot and prolifera

180 that period, pollen allergic as well as non-allergic patients frequently present to doctors with sev

181 Reported BL allergic patients have an increased odds of developing S

182 Immunoblot assays performed with fish-allergic patients sera indicated a 50% reduction in IgE-

183 ut-specific CD4(+) T-cell response in peanut-allergic patients that correlate with high clinical sens

184 ers (n = 6, healthy controls; n = 14, peanut-allergic patients) at various time-points following inge

185 A diary score of symptoms was collected from allergic patients.

186 hours after nickel patch test in six nickel-allergic patients.

187 reting Th cells were high in house dust mite-allergic patients.

188 odds of developing SSI in comparison to NBL allergic patients.

189 We conclude that the allergic phenotype has likely saved the lives of many mo

190 ion of health utility from the Canadian food-allergic population.

191 he prevalence rates of personal history with allergic proctocolitis (23.2%) and family history with i

192 ted allergy, outside of food protein-induced allergic proctocolitis and eosinophilic oesophagitis, is

193 In recent years, a major role for IL-31 in allergic pruritus of humans, monkeys, dogs, and mice was

194 Anaphylaxis is a severe allergic reaction that can be lethal if not treated adeq

195 n acute, potential life-threatening systemic allergic reaction that may have a wide range of clinical

196 One adverse event (an allergic reaction) was reported in 1 patient in the PPI

197 ved HCP advice/support following their worst allergic reaction, and 28% had not been prescribed an ad

198 Outcome measures included allergic reactions (ie gastrointestinal, dermatological,

199 Immunoglobulins E (IgEs) trigger allergic reactions by specifically binding the allergens

200 ntify the allergens responsible for systemic allergic reactions following ingestion of pizza in two p

201 rate that EPIT markedly reduced IgE-mediated allergic reactions in a mouse model of cashew allergy, w

202 anut allergy (PA), but it involves a risk of allergic reactions of unpredictable severity.

203 No patients exhibited any systemic or local allergic reactions or complications after intravitreal i

204 s underlying the variable severity of peanut-allergic reactions remain unclear.

205 st cells (MCs) are central effector cells in allergic reactions that are often mediated by immunoglob

206 this cohort have become especially aware of allergic reactions to food.

207 Unexpected allergic reactions to peanut are the most common cause o

208 he discrepancy between IgE sensitization and allergic reactions to peanut could facilitate diagnosis

209 o PA status, severity, and threshold dose of allergic reactions to peanut during OFC.

210 of allergenic foods and management of acute allergic reactions with antihistamines and epinephrine a

211 is one of the most common elicitors of food-allergic reactions worldwide.

212 ntal (47.6%) and self (21.8%) concerns about allergic reactions, lack of referrals (33.6%), parents u

213 is, a severe life-threatening consequence of allergic reactions.

214 ) syndrome, which is characterized by severe allergic reactions.

215 winia) substitution was approved in 2011 for allergic reactions.

216 f food allergens may be a key determinant of allergic reactions.

217 reatment with butyrate significantly reduced allergic response in three animal models of FA, with a s

218 d a week earlier is sufficient to trigger an allergic response-but only if participants had slept aft

219 ell degranulation is a critical component of allergic response.

220 teolytic activity contributes to the overall allergic response.

221 ed ceramide levels in the lung contribute to allergic responses and asthma severity.

222 Geha, they studied the role of Th2 cells in allergic responses and he began work in Kawasaki's disea

223 t have important roles in the development of allergic responses as well as the body of evidence on en

224 Our findings provide evidence that allergic responses can be conditioned to contextual info

225 Allergies are highly prevalent, and allergic responses can be triggered even in the absence

226 wild-type mice, iTreg cells suppressed lung allergic responses linked to Smad3-dependent forkhead bo

227 tions between them are essential to maximize allergic responses.

228 me pathogenic effector cells, enhancing lung allergic responses.

229 n part of the strong psychological impact on allergic responses.

230 ight be a mechanism to suppress IgE-mediated allergic responses.

231 ss to adenosine, could be useful to suppress allergic responses.

232 Allergic rhinitis (AR) and local allergic rhinitis (LAR)

233 f asthma whereas evidence for remodelling in allergic rhinitis (AR) is conflicting.

234 ents who received at least three symptomatic allergic rhinitis (AR) prescriptions in successive mite

235 unotherapy (AIT) prevents the progression of allergic rhinitis (AR) to asthma.

236 es and subsequent risk for diseases, such as allergic rhinitis (AR).

237 Allergic rhinitis (AR) and local allergic rhinitis (LAR) are defined by nasal reactivity

238 s in a panel study of subjects with seasonal allergic rhinitis (SAR) and subjects without allergy and

239 sis (asthma aOR = 2.61 [95% CI = 2.14-3.18]; allergic rhinitis aOR = 1.96 [95% CI = 1.58-2.42]; eosin

240 were collected from 40 adults with seasonal allergic rhinitis at baseline and at 4, 8, 16, 28, and 5

241 We propose the term dual allergic rhinitis for this rhinitis phenotype.

242 The prevalence of allergic sensitisation and allergic rhinitis increased in a general adult Danish po

243 shows that families with eczema, asthma, or allergic rhinitis should not use daily emollients to try

244 Here we show in humans suffering from allergic rhinitis that merely reencountering the environ

245 Allergic rhinitis to grass pollen (ARg) was defined as u

246 Allergic rhinitis was defined as sensitisation and self-

247 d with allergic disease (asthma, eczema, and allergic rhinitis) and corticosteroid use.

248 for specific areas of allergology, including allergic rhinitis, aerobiology, allergen immunotherapy,

249 led that Down syndrome, astigmatism, myopia, allergic rhinitis, and asthma were positively associated

250 ergic diseases, including atopic dermatitis, allergic rhinitis, and asthma.

251 morbidities, including food allergy, asthma, allergic rhinitis, and mental health disorders.

252 Rates of allergic rhinitis, asthma and other food allergies in Pw

253 roallergen sensitization, atopic dermatitis, allergic rhinitis, asthma, and challenge-proved food all

254 e to develop chronic inflammation as seen in allergic rhinitis, chronic rhinosinusitis, and asthma.

255 Clinical factors, including asthma, allergic rhinitis, eosinophil count of at least 150 cell

256 Asthma, allergic rhinitis, eosinophil count of at least 150 cell

257 diseases such as atopic dermatitis, asthma, allergic rhinitis, food allergy, contact allergy, and ha

258 degree relative with parent-reported eczema, allergic rhinitis, or asthma, diagnosed by a doctor).

259 lls from children and adults with asthma and allergic rhinitis.

260 an effective, safe treatment for HDM-induced allergic rhinitis.

261 outcome assessment in patients with seasonal allergic rhinitis.

262 d adults with moderate to severe HDM-induced allergic rhinitis.

263 ns in nasal secretion (r = 0.69, P = .06) in allergic rhinitis.

264 No subject had a history of asthma/allergic rhinitis: all had negative results for aeroalle

265 potential benefit of dupilumab in perennial allergic rhinoconjunctivitis (PAR) and perennial allergi

266 Allergic rhinoconjunctivitis is a global health problem.

267 The prevalence of allergic sensitisation and allergic rhinitis increased i

268 Allergic sensitisation was defined by sIgE (in 1990-1991

269 mouse model of house dust mite (HDM)-induced allergic sensitization and allergic airway inflammation.

270 mice, only treatments with holoBLG prevented allergic sensitization and anaphylaxis, while sustaining

271 or development of atopic dermatitis; data on allergic sensitization and asthma were collected when ch

272 llular interactions that are associated with allergic sensitization and clinical food allergy in the

273 The immune states that predispose towards allergic sensitization and disease development remain il

274 he impact of an epithelial barrier defect on allergic sensitization and mast cell (MC) degranulation

275 Allergic sensitization is associated with severe asthma,

276 atios were higher among participants without allergic sensitization than among those with, but intera

277 reasing evidence regarding the importance of allergic sensitization through the skin.

278 The predisposition to allergic sensitization was associated with increased air

279 transepidermal water loss and allergic sensitization were assessed.

280 re at a significantly higher risk developing allergic sensitization(OR [95% CI] = 2.00 [1.04:3.86] at

281 acilitates transepithelial allergen passage, allergic sensitization, and allergen-induced MC degranul

282 iated with development of atopic dermatitis, allergic sensitization, and asthma.

283 vented chitosan-induced barrier dysfunction, allergic sensitization, and MC degranulation.

284 n was evaluated in a murine model of Phl p 5 allergic sensitization.

285 lative to skin transepidermal water loss and allergic sensitization.

286 ctory was associated with the early onset of allergic sensitization.

287 oes not seem to increase the overall risk of allergic sensitization; however, sensitization to birch

288 allergens, linking exposure to activation of allergic-skewing DCs and the initiation of an allergic i

289 Sera from almond-allergic subjects had significantly higher IgE levels to

290 ophils sensitized with plasma from alpha-gal allergic subjects in an IgE-dependent manner suggesting

291 thms and administration of alternative BL in allergic subjects.

292 Both treatment of allergic symptoms and prevention of future anaphylactic

293 es in 785 case patients and 2124 controls by allergic symptoms only from 8 cohorts, 3 of which were n

294 IgE reactivity analysis in 28 patients allergic to chicken meat revealed that Gal d 7 is a majo

295 component is observed in young pigs rendered allergic to hen egg white protein (HEWP).

296 of endotoxin-stimulated PBMCs from children allergic to milk or egg, but not peanut, were significan

297 Among children allergic to unbaked egg but tolerant to BE, those treate

298 estion compared with egg OIT in participants allergic to unbaked egg but tolerant to BE.

299 of the factors that predispose to different allergic trajectories is needed.

300 d huFcepsilonRIalpha/F709 mice that were egg-allergic with anti-FcepsilonRIalpha mAbs safely removed