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1  route of allergen exposure (inhaled vs food allergens).
2 his band we identified was a novel enokitake allergen.
3 e association with low IgE reactivity to any allergen.
4 ansgenic 1-DER mice specific for the Der p 1 allergen.
5 ermates following intranasal exposure to HDM allergen.
6 noblotting to screen for potential bacterial allergens.
7 d still unavailable important cross-reacting allergens.
8 P ISAC((R)) for IgE reactivity to 112 single allergens.
9 s commercial extracts as well as recombinant allergens.
10 itive to the ImmunoCAP ISAC for various food allergens.
11 ion that occurs in response to environmental allergens.
12 tization profile and reacted on average to 9 allergens.
13  microbes, injuries, solar UV radiation, and allergens.
14 med at modifying the response to sensitizing allergens.
15 l symptoms and sensitization status to major allergens.
16 n host responses to pathogens, parasites and allergens.
17  to prevent unwanted reactions against minor allergens.
18 ling moisturizer products were free of NACDG allergens.
19 the heterogeneity of T cell responses to HDM allergens.
20  TOT fraction was the richest in the Amb a 8 allergens (89% and 83% of allergome, respectively).
21 concurrent elevated specific IgE against any allergen [adjusted OR (aOR) = 1.40; 95% CI, 1.14-1.72; P
22 C2) and eosinophilic responses to Alternaria allergen administration, and diminished eosinophilic res
23 nfluence of environmental exposures, such as allergens, air pollution, and the environmental microbio
24                   Concentrations of 8 indoor allergens (Alt a 1, Bla g 1, Can f 1, Fel d 1, Der f 1,
25  ILC2 responses after exposure to the fungal allergen Alternaria alternata Thus, CysLT1R promotes LTC
26 ng type 2 inflammation induced by the fungal allergen Alternaria alternata.
27 contain five different isoforms of the major allergen Amb a 1.
28             However, the sequential order of allergen and adjuvant within a fusion protein determines
29  M2 polarization in vivo upon challenge with allergen and that macrophage-specific deletion of ERalph
30 sociated with IgE sensitization to both food allergens and aeroallergens up to age 16 years (overall
31 ociation of geographical areas with relevant allergens and allergic clinical picture.
32  and glycan-specific IgE on sensitization to allergens and allergy diagnosis is described.
33 gests limited cross-reactivity between these allergens and Blo t 1.
34 t that diverse biologic exposures, including allergens and endotoxin, in urban homes stimulate the de
35 k-related asthma patients exposed to protein allergens and isocyanates elicit similar nasal proteome
36  we define the T cell targets for both known allergens and novel proteins, which may inform future di
37 ry tissue exposed to inhaled microorganisms, allergens and pollutants.
38 ral tolerance induction to other common food allergens and that focus on optimal timing, duration, an
39 t debut, development over time, and involved allergens and that such patterns might be more biologica
40 unclear whether these products are free from allergens and therefore safe to consume or have simply n
41 ities of the minor Amb a 4 and major Amb a 1 allergens, and as unique, NADH dehydrogenases.
42 rch pollen allergen, its cross-reactive food allergens, and profilins.
43 -resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations.
44 gens (aOR, 1.43; 1.15-1.77; P = 0.001), food allergens (aOR, 1.31; 95% CI, 1.02-1.67; P = 0.04), sens
45            Based on the fact that intranasal allergen application induces rises of systemic allergen-
46 to allergen risk management, even when these allergens are heat-processed into baked foods.
47 s an extension of PERFILAR I with additional allergens being included.
48 eins of flagellin and the major birch pollen allergen Bet v 1 for suitability as allergy vaccines.
49  By using a human IgE mAb, the corresponding allergen Bet v 1, and a panel of antibodies specific for
50 ranasal administration of major birch pollen allergen Bet v 1, omalizumab or placebo on the levels of
51 lly with omalizumab, placebo or birch pollen allergen Bet v 1.
52 egarding IgE to major birch and grass pollen allergens Bet v 1 and Phl p 1/p 5 and the profilins Bet
53 t (P < .001) dose-dependent reduction in IgE allergen binding across all treatment groups (70 mug: 17
54 rgen-IgE binding to B cells (IgE-facilitated allergen binding).
55                                  Facilitated allergen-binding assays revealed a highly significant (P
56   Despite highly variable exposures, bedroom allergen burden is strongly associated with the presence
57 ost importantly, recognition of encapsulated allergen by the immune system, especially by IgE antibod
58         The availability of recombinant food allergens can accelerate their structural analysis and b
59 lying that existing threshold data for these allergens can be applied to allergen risk management, ev
60              Cellulose used as a solid-phase allergen carrier can contain varying amounts of CCDs suf
61                                        Nasal allergen challenge (NAC) is a human model of allergic rh
62 ing at sites of inflammation after segmental allergen challenge (SAC).
63 lergy reduced anaphylactic responses to oral allergen challenge by 84% to 90%, as well as diarrhea, m
64 ronchoalveolar lavage fluid, after segmental allergen challenge in allergic asthmatic patients.
65 granulation, and allergic symptoms caused by allergen challenge in sensitized mice.
66 enous injection of IL-33 or pulmonary fungal allergen challenge mobilized ILC2 progenitors to exit th
67                 We used a human experimental allergen challenge model, with flow cytometric analysis
68             TNF was also required during the allergen challenge phase for neutrophilic and eosinophil
69  inhibitor (Compound 20) administered during allergen challenge reduced ILC2 numbers and activation,
70                                              Allergen challenge resulted in airway inflammation as ev
71                                              Allergen challenge was continued during HOCl hydrogel ap
72                                        Nasal allergen challenge was performed before treatment, at 1
73                                     After an allergen challenge, subjects with atopy displayed rapid
74 d airway hyperresponsiveness (AHR) following allergen challenge, whereas mice sensitized using protea
75 ed with macrophages from male mice following allergen challenge.
76 es and neutrophil/lymphocyte ratio after the allergen challenge.
77 ion in airway hyperresponsiveness (AHR), OVA allergen-challenged Ormdl3(Delta2-3/Delta2-3)/CC10 mice
78       As shown here, eosinophils from fungal allergen-challenged wild-type mice maintain a distinct c
79 eosinophil cultures from the lungs of fungal allergen-challenged wild-type mice.
80                                        Nasal allergen challenges (NACs) and allergic biomarker assess
81 y specimens were collected after intradermal allergen challenges, and late-phase responses were measu
82                          Exposure to certain allergens (cockroach, mouse, dust mite) was significantl
83 plicity of sensitization (food vs inhalant), allergen combinations, and sIgE levels.
84  bronchial inflammation when challenged with allergen compared to negative controls.
85 gE and IgG responses to 47 inhalant and food allergen components were analyzed in sera using allergen
86 eptor (FcRn)-mediated transfer and uptake of allergen-containing IgG immune complexes (Ig-ICs) by gut
87                        Cockroach, like other allergens, contains trypsin-like enzyme activity that co
88 lysis assessed homologies between virus- and allergen-derived proteins.
89                                              Allergen detection in 2D-Western blots with PBS resulted
90 tection limit achieved exceeded the required allergens detection levels of 2microgmL(-1) for alpha-S1
91 f sifter, and measured the distance of wheat allergen dispersal over 20 minutes using a petri dish an
92 ssociated food allergies, a single wild-type allergen does not provide a complete solution.
93  based on FcepsilonRI occupancy with IgE and allergen dose.
94 n 5 French regions according to the route of allergen exposure (inhaled vs food allergens).
95  mucosal cytokine responses induced by nasal allergen exposure and humoral immune responses that incl
96                                              Allergen exposure chambers (AECs) are clinical facilitie
97                                          Dog allergen exposure did not show such interaction.
98                         Indoor environmental allergen exposure during early life can also affect dise
99                                    Dust mite allergen exposure modifies the estimated effect of rs117
100 the present study, we examined the effect of allergen exposure on TREM-2 expression in the airways an
101 Allergic airway inflammation is triggered by allergen exposure through several steps including releas
102 ed increased CCR5 expression after high-dose allergen exposure while CXCR4, CXCR5, CCR6, and CCR7 exp
103 xhibited increased airway inflammation after allergen exposure, with massive eosinophilic lung infilt
104 in early life to induce persistent AHR after allergen exposure.
105 nd climatic factors, associated with bedroom allergen exposures in a nationally representative sample
106 rved in human subjects as the consequence of allergen exposures that recurrently activate memory B ce
107                              In this region, allergen extract-based diagnosis is often complicated by
108                       German cockroach (GCr) allergen extracts are complex and heterogeneous products
109 With respect to assay performance, ImmunoCAP allergen extracts are good screening tools, but allergen
110   In addition, we discuss of house dust mite allergen extracts as a prototypical complex extract that
111 d to ensure the availability of high-quality allergen extracts to maintain the common diagnostic proc
112 d to the conventional AIT with noncapsulated allergen extracts: The protein/DNA molecule can be prote
113 ins such as ovalbumin (OVA) or the major cat allergen Fel d 1.
114        Extensive chemical processing ensures allergen-free pollen microcapsules that can be loaded wi
115 e report the crystal structure of one of the allergens from Blo t, recombinant proBlo t 1 (rproBlo t
116 tablished a comprehensive peptide library of allergens from various commercial extracts as well as re
117          The extraction of Ara h 6 (a peanut allergen) from a complex chocolate-based food matrix was
118    On the other hand, the IgE-binding glycan allergen galactose-alpha-(1,3)-galactose (alpha-Gal) is
119                         The most common food allergen groups were shellfish (0.9%), fruit or vegetabl
120 the proteolytic activity of German cockroach allergen have not been characterized.
121 g to the helminth Schistosoma mansoni or the allergen house dust mite (HDM).
122                                  Among known allergens, hydrolase activity and detectable IgE/IgG rea
123             However, tolerance is brief, and allergen hypersensitivity can recur within days followin
124                   For ubiquitous respiratory allergens (ie, grass, olive/ash pollen, house dust mites
125 measurement of serum inhibitory activity for allergen-IgE binding to B cells (IgE-facilitated allerge
126 ortantly, FcepsilonRII-mediated signaling by allergen-IgE immune complexes increased IFN-gamma produc
127                                  Defined IgE-allergen immune complexes were formed with human monoclo
128                                              Allergen immunotherapy (AIT) is a form of treatment spec
129 Guidelines and position papers indicate that allergen immunotherapy (AIT) is the only disease-modifyi
130 iew, we report on relevant current topics in allergen immunotherapy (AIT) which were broadly discusse
131 mmunology (EAACI) has produced Guidelines on Allergen Immunotherapy (AIT).
132     Most of the SRs occurred in subcutaneous allergen immunotherapy (SCIT) (89%, n = 97).
133                          Studies with pollen allergen immunotherapy are limited to observational stud
134  cancer progression, whereas on the contrary allergen immunotherapy exactly aims to induce tolerance.
135                         A novel subcutaneous allergen immunotherapy formulation (gpASIT+) containing
136      CLINICAL IMPLICATIONS: We here evaluate allergen immunotherapy guideline (AIT-GL) quality.
137                         Since 1988, numerous allergen immunotherapy guidelines (AIT-GLs) have been de
138 notherapy as part of the EAACI Guidelines on Allergen Immunotherapy initiative.
139                                              Allergen immunotherapy is effective in patients with IgE
140                                              Allergen immunotherapy, the aetiological treatment for a
141 s that may affect the efficacy and safety of allergen immunotherapy.
142 omega-5 gliadin fraction, is the most common allergen implicated in food-dependent, exercise-induced
143 apid and sensitive on-site detection of milk allergen in food stuff.
144 city students with asthma, exposure to mouse allergen in schools was associated with increased asthma
145 owing for controlled exposure of subjects to allergens in an enclosed environment.
146                Dose-response curves with the allergens in BAT allowed a differentiated individual dis
147                      Exposure to dog and cat allergens in DCC often reached levels of households with
148 pecific for staple foods and house dust mite allergens in DOCK8-deficient patients and healthy contro
149 sues affecting studies of AIT with perennial allergens in patients with AA and AR, including use of d
150  to 2 kUA/L with nonglycosylated recombinant allergens in patients with high levels of anti-CCD IgE a
151                 Intranasal administration of allergen induced rises of allergen-specific IgE levels,
152 on of proinflammatory cytokines and improves allergen-induced AHR, airway resistance, and compliance.
153 nts, both cell types enhanced development of allergen-induced airway hyperresponsiveness.
154                         Airway tolerance and allergen-induced airway inflammation models in mice were
155          Lyn has been shown to down-regulate allergen-induced airway inflammation.
156 in reinstatement of susceptibility to fungal allergen-induced allergic airways disease.
157 a novel treatment strategy for children with allergen-induced asthma.
158 ur knowledge, we show that rfhSP-D inhibited allergen-induced basophil responses at a single-cell lev
159 lymph nodes and prevented IgE-dependent oral allergen-induced diarrhea.
160 p quality participates in the progression of allergen-induced eosinophilic lung inflammation to corti
161                                   We studied allergen-induced experimental asthma in ST2 knockout (KO
162 rface hydration and mucus clearance, reduced allergen-induced inflammation in Scnn1b-Tg mice.
163 (WT) mice were subjected to acute or chronic allergen-induced inflammation or treated with recombinan
164  (TLR) 2, TLR4 and MyD88, in exacerbation of allergen-induced lung eosinophilia caused by urban PM2.5
165 We sought to evaluate the influence of SD on allergen-induced pulmonary inflammation.
166 th total IgE levels (RS = 0.53, P = .03) and allergen-induced skin reactions (RS = 0.63, P = .008).
167 aired mucus clearance in the pathogenesis of allergen-induced type 2 airway inflammation and identify
168                   Exposure of these cells to allergens induces the release of soluble mediators causi
169  for allergic reactions caused by accidental allergen ingestion in this group.
170 hinitis to receive 7 preseasonal intradermal allergen injections (containing 7 ng of Phl p 5 major al
171 , we wanted to investigate whether hen's egg allergen is detectable in house dust collected from diff
172 gen, particularly when the amount of inhaled allergen is low, by expanding allergen-specific T cells.
173                         Exposure to multiple allergens is common.
174 itization to Bet v 1, the major birch pollen allergen, its cross-reactive food allergens, and profili
175                   Profilins are dominant pan-allergens known to cause cross-sensitization, leading to
176 lf the group reported ignoring precautionary allergen labeling.
177                            The precautionary allergen labelling (PAL) and Voluntary Incidental Trace
178 belling (PAL) and Voluntary Incidental Trace Allergen Labelling (VITAL((R)) ) tools were designed by
179 e sensor would be useful tool for monitoring allergen levels after cleaning procedures, providing add
180 and dog ownership from birth and cat and dog allergen levels in bedding at age 1 year.
181                                Influences on allergen levels were analyzed using multilevel models.
182                                              Allergen levels were significantly influenced by the sea
183 th FEV1 in children exposed to low dust mite allergen levels, but negatively associated with FEV1 in
184                                              Allergen loads were on average higher in DCC than in hom
185 gic rhinitis (AR) that delivers standardized allergens locally to the nasal mucosa allowing clinical
186 merican Contact Dermatitis Society's Contact Allergen Management Program database.
187 ergen components were analyzed in sera using allergen microarray and compared between 5 French region
188       Furthermore, little is known about the allergen molecules causative for type I food allergy in
189 ergen extracts are good screening tools, but allergen molecules dissect the IgE response on a molecul
190                          The introduction of allergen molecules has had a major effect on analytic sp
191 volution of the IgE response to the numerous allergen molecules of Dermatophagoides pteronyssinus is
192       This leads to the assumption that food allergens must have specific structural features which c
193     This information can be used to engineer allergen mutants with reduced IgE Ab binding for immunot
194 plays several characteristics of sensitizing allergens, namely a major T-cell-activating region, low
195 n of the clinically relevant and sensitizing allergen needs correlation of actual pollen counts with
196 fficially indexed as Cup s 2 by the WHO/IUIS allergen nomenclature.
197 Tcon cells were cocultured with SEA-reactive allergen-nonspecific Treg or CD4 Tcon cells in the prese
198 he S aureus-derived protein SplD is a potent allergen of S aureus and induces a TH2-biased inflammato
199                         However, the driving allergens of S aureus have remained elusive.
200 isplaying a weak cross-reactivity with other allergens of the PR-10 family.
201 ite residual binding, repetitively displayed allergen on VLPs failed to cause mast cell activation.
202 ndings indicate that repetitively displaying allergens on VLPs increases their immunogenicity while r
203                             Encapsulation of allergens or DNA vaccines into nanostructures may provid
204 injections (containing 7 ng of Phl p 5 major allergen) or a histamine control.
205 zation and desensitization to the model food allergen ovalbumin.
206                After exposure to the natural allergen papain, mice selectively lacking the miR-17 app
207  the adaptive immune response to inhaled HDM allergen, particularly when the amount of inhaled allerg
208  PTC) occurred across days 2 to 4 with grass allergen peptide 8x6Q2W versus placebo (-5.4 vs -3.8, re
209 r improvement at PTC also occurred for grass allergen peptide 8x6Q2W versus placebo (P = .0403) in pa
210 towards Phl p 12 are comparable to the major allergen Phl p 1, which supports the hypothesis that T c
211 re prone to extensive cross-reactivity among allergen pollen extracts.
212           Early-life sensitization to indoor allergens predicts asthma development.
213 vel and suppressed CD23-mediated facilitated allergen presentation and Th2 cytokine production.
214                         Delivery of specific allergen-presenting DC-RAs to half-maximally sensitized
215 ic disease and necessitates the avoidance of allergens, prevention of infections, adherence with rout
216 ring AIT with birch pollen were added to the allergen prior to intranasal challenge.
217 s show marked differences in specific peanut allergen profiles in peanut butter and flour and peanut
218  Quality of Life Questionnaire (RQLQ), nasal allergen provocation test (NAPT), skin testing, serum le
219                                        Nasal allergen provocation tests (NAPT) with Dermatophagoides
220 bjects with atopy and healthy subjects after allergen provocation.
221                                          The allergen Pru p 3, a peach lipid transfer protein, has be
222  and thermal processing of peanuts perturbed allergen quantification in ELISAs, probably via exposure
223 c(-/-) (NSG) mice received intraperitoneally allergen-reactive PBMC from birch pollen-allergic patien
224 Sema3E on cytokine response was sustained on allergen recall response in the lymph nodes and spleen.
225               We identify Spls as triggering allergens released by S aureus, opening prospects for di
226           Depletion of NK cells restored the allergen responsiveness in the lungs and was associated
227  data that may better inform upon wider food allergen risk management decision(s) that are made by fo
228 d data for these allergens can be applied to allergen risk management, even when these allergens are
229                    To study whether maternal allergen sensitization affects offspring susceptibility
230 nomodulators showed reduced anaphylaxis upon allergen sensitization and challenge, irrespective of th
231 e exaggerated bronchoconstriction induced by allergen sensitization and challenge.
232  the host response is affected by subsequent allergen sensitization and exposure.
233                                              Allergen sensitization and high frequencies of comorbid
234 ia PAR2 activation, play different roles for allergen sensitization in vivo and may represent attract
235 tive effects of CpG when administered before allergen sensitization or challenge.
236 netic and sociocultural characteristics, but allergen sensitization shows wide geographical variation
237  study incidence and persistence of airborne allergen sensitization up to young adulthood and risk fa
238 ow skin barrier defects can lead to systemic allergen sensitization.
239 of life were assessed along with patterns of allergen sensitization.
240  was the risk difference in the onset of new allergen sensitizations between patients treated with AI
241 nt, including prevention of the onset of new allergen sensitizations.
242 e selective CysLT2R agonist N-methyl LTC4 to allergen sensitized wild-type mice markedly boosted ILC2
243 ness, and airway remodeling were analyzed in allergen-sensitized and airway-challenged mice.
244 he transfer of eosinophils from the lungs of allergen-sensitized and challenged mice into influenza v
245 G) milk protein, one of the most common food allergens specially in infants.
246 formed multimodal immunomonitoring to assess allergen-specific CD4 T-cell properties in parallel with
247 mination at age 2 years to assess eczema and allergen-specific IgE (sIgE) and perform skin prick test
248  complexes were formed with human monoclonal allergen-specific IgE and Bet v 1.
249 -MAPS) to the simultaneous detection of food allergen-specific IgE and IgG4 , and compared it with Im
250                                              Allergen-specific IgE antibodies are a hallmark of type
251 izumab or placebo on the levels of total and allergen-specific IgE in patients with birch pollen alle
252  administration of allergen induced rises of allergen-specific IgE levels, whereas intranasal adminis
253 omalizumab did not enhance systemic total or allergen-specific IgE levels.
254                               Examination of allergen-specific IgE revealed plasma IgE from DOCK8-def
255                                   Binding of allergen-specific IgE to its high-affinity receptor Fcep
256                                    Total and allergen-specific IgE, IgG and basophil sensitivity were
257 lergen application induces rises of systemic allergen-specific IgE, we performed a double-blind place
258 vation, and TH2 cytokine responses and serum allergen-specific IgE/IgG1 levels.
259         Animal models have demonstrated that allergen-specific IgG confers sensitivity to systemic an
260                                              Allergen-specific IgG was administered to mice undergoin
261      It is recommended to explore the use of allergen-specific IgG4 as a biomarker for compliance.
262 ted with characteristic modifications in the allergen-specific immune response, but a detailed synthe
263 ggest for the use as adjuvant and carrier in allergen-specific immunotherapy (ASIT).
264                                  The goal of allergen-specific immunotherapy is the induction of prot
265 lergic patients during the build-up phase of allergen-specific immunotherapy.
266  fusion proteins can enhance the efficacy of allergen-specific immunotherapy.
267 Instead, lifelong reactivity is conferred by allergen-specific long-lived memory B cells that repleni
268                  Altogether, we believe that allergen-specific memory T cells reside and function in
269 es (IgG-IC) via breast milk and induction of allergen-specific regulatory T (T reg) cells in offsprin
270 surements including positive SPT or elevated allergen-specific serum/plasma IgE levels.
271 sitive skin prick testing (SPT), or elevated allergen-specific serum/plasma immunoglobulin (Ig) E lev
272                SEA promoted TH2 responses of allergen-specific T cells and asthma pathogenesis by act
273 unt of inhaled allergen is low, by expanding allergen-specific T cells.
274      The marked increase in APC function for allergen-specific TC proliferation during allergic infla
275                                              Allergen-specific TH2 cells most closely paralleled the
276      Beside avoidance, there is currently no allergen-specific therapy available.
277   In allergic asthma, inhalation of airborne allergens such as the house dust mite (HDM) effectively
278  53.5% showed IgE reactivity to at least one allergen tested.
279 e-containing parts on each of the 3 parental allergens, the hybrid molecule was designed to cover rel
280 rgy in humans has been well studied for some allergens, this remains to be investigated for animal pa
281 ve mice were exposed to cytokines or natural allergens through the airways.
282 nt) DC-RAs were ineffective in inducing food allergen tolerance.
283 olved in the regulation of IgE synthesis and allergen transcytosis.
284                       Effective diaplacentar allergen transfer was detectable in pregnant WT mice but
285 eral control groups (nonallergic, history of allergen-triggered anaphylaxis, acute cardiovascular/feb
286 a support that impaired clearance of inhaled allergens triggering IL-13 production by multiple cell t
287 affect disease development, depending on the allergen type, dose, and timing of exposure.
288 extract, yet was facilitated by applying the allergen under an occlusive tape.
289  stability of enzymatic activities and major allergens under stress conditions (40 degrees C) has bee
290 llergy and accompany the acquisition of food allergen unresponsiveness in oral immunotherapy.
291 itization and challenge, irrespective of the allergen used.
292 nsitization to at least one food or inhalant allergen was found in 319 of 765 (41.7%), and to at leas
293 Sublingual treatment with a recombinant food allergen was safe and clinically effective, as determine
294 ifferences, high exposure burden to multiple allergens was most consistently associated with the pres
295 n analysis of antigenic determinants on both allergens was performed by site-directed mutagenesis.
296                                     Seasonal allergens were associated with rhinitis, a longer time t
297 o 4) and binding to a panel of 4 recombinant allergens were compared in CCD-positive sera before and
298                          During endoscopy, 6 allergens were injected in the esophagus of 8 patients w
299                        MBC4 and the parental allergens were purified to homogeneity.
300 relevant for IL-4-dependent IgE responses to allergens with the amount of IL-4 produced in the hemizy
301 rsensitivity can recur within days following allergen withdrawal.

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