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1 articipated in a mouse model of NO2-promoted allergic sensitization.
2 ntation and asthma exacerbations, eczema, or allergic sensitization.
3 pe of enhanced eosinophilic inflammation and allergic sensitization.
4 thought to be crucial for the development of allergic sensitization.
5 re of B cells to pollen constituents affects allergic sensitization.
6 that PAR2 activation in the airways leads to allergic sensitization.
7 mportant tools for the clinician to diagnose allergic sensitization.
8  to control oxidative stress might prime for allergic sensitization.
9 concurrent with antigen exposure accelerated allergic sensitization.
10 initiators of atopic dermatitis and possibly allergic sensitization.
11 ted by commensal bacteria to protect against allergic sensitization.
12 ons with self-reported allergic rhinitis and allergic sensitization.
13 re least likely to have recurrent wheeze and allergic sensitization.
14 ion was not found between TSLP and eczema or allergic sensitization.
15 hinitis from 10 to 16 years, stratifying for allergic sensitization.
16 n the quantity of LPS inhaled at the time of allergic sensitization.
17 sive circumstances, mount a Th2 response for allergic sensitization.
18 boratory animals is useful for understanding allergic sensitization.
19 he involvement of Treg in the suppression of allergic sensitization.
20 eding in MCT-based diets, caused spontaneous allergic sensitization.
21 lergen was associated with a greater risk of allergic sensitization.
22 rbons (PAHs), can augment the development of allergic sensitization.
23 es in models of infection, autoimmunity, and allergic sensitization.
24 t of childhood asthma, wheeze, rhinitis, and allergic sensitization.
25 nt of the lung and reducing the intensity of allergic sensitization.
26 s are associated with a reduced incidence of allergic sensitization.
27   Neonatal size did not associate with AD or allergic sensitization.
28 rested in determining their association with allergic sensitization.
29 are thought to contribute to helminth-driven allergic sensitization.
30  parabens were significantly associated with allergic sensitization.
31 ot correlate consistently with indicators of allergic sensitization.
32 and SE sensitization to allergic disease and allergic sensitization.
33               This effect was independent of allergic sensitization.
34 gands, but not proteases, induced TNF during allergic sensitization.
35 5% CI: 1.21-37.74), but not among those with allergic sensitization.
36 ed TH2 inflammation but does not prevent the allergic sensitization.
37 gate the possible association with childhood allergic sensitization.
38 elopment of recurrent wheezing illnesses and allergic sensitization.
39 sm, but is largely unexplored in relation to allergic sensitization.
40 ggered by distinct types of adjuvants during allergic sensitization.
41 ciation with childhood allergic rhinitis and allergic sensitization.
42 nfections, asthma exacerbations, eczema, and allergic sensitization.
43 fraction of exhaled nitric oxide (Feno), and allergic sensitization.
44  (95% CI: 1.02, 1.33), 1.20 for any specific allergic sensitization (95% CI: 1.05, 1.37), and 1.43 fo
45 5% CI: 1.05, 1.37), and 1.43 for tree pollen allergic sensitization (95% CI: 1.19, 1.72).
46 fic immune deviation than via suppression of allergic sensitization, a mechanism to be considered in
47                                              Allergic sensitization against 28 inhalant and food alle
48                                              Allergic sensitization against common inhalant and food
49                                        Early allergic sensitization (aHR, 4.53; 95% CI, 3.25-6.32), e
50 re noted on the effect of a viral infection, allergic sensitization, airway inflammation and airway h
51 er function of airway epithelium, leading to allergic sensitization, airway remodeling, and eosinophi
52      Environmental tobacco exposure, but not allergic sensitization, also hampered airflow growth.
53 ve studies on the incidence and remission of allergic sensitization among adults are rare.
54    Early onset of asthma was associated with allergic sensitization among adults with asthma.
55                            The prevalence of allergic sensitization among patients with asthma decrea
56                   Thus the low prevalence of allergic sensitization among the elderly found in cross-
57            The adjusted odds ratio (aOR) for allergic sensitization among those in the fourth quartil
58 tion, inflammatory chemokine production, and allergic sensitization and airway inflammation suggest t
59 models exposure to endotoxin (LPS) decreases allergic sensitization and airway inflammation.
60                   RWPE induced MD2-dependent allergic sensitization and airway inflammation.
61 ilic inflammation, which in turn facilitates allergic sensitization and airway inflammation.
62 ocation of Treg cell function differs during allergic sensitization and allergen-induced recall respo
63  among the most common allergens that induce allergic sensitization and allergic diseases.
64 ere estimated to account for at least 25% of allergic sensitization and allergic rhinitis.
65 k and mature milk and to investigate whether allergic sensitization and an anthroposophic lifestyle c
66 everity are an allergy pathway starting with allergic sensitization and an environmental tobacco smok
67                         Dietary MCTs promote allergic sensitization and anaphylaxis by affecting anti
68 ogic data describing the association between allergic sensitization and asthma and allergic rhinitis
69 sed no detectable changes, it did exacerbate allergic sensitization and asthma characteristics to a s
70 nt of immune function, and predisposition to allergic sensitization and asthma.
71 t allergens, Der p 1 and Der f 1, that cause allergic sensitization and asthma.
72 en associated with subsequent development of allergic sensitization and asthma.
73 hanisms regarding cockroach allergen-induced allergic sensitization and asthma.
74                                              Allergic sensitization and atopic dermatitis (AD) were a
75  that influence the development of childhood allergic sensitization and atopic diseases.
76                                 In addition, allergic sensitization and blood eosinophils can be used
77 ased the inflammatory response to subsequent allergic sensitization and challenge.
78 f immunomodulatory T cell characteristics to allergic sensitization and disease at 1- and 2-years of
79  years of life have been linked with risk of allergic sensitization and disease.
80 tective role of breastfeeding in relation to allergic sensitization and disease.
81                                              Allergic sensitization and diseases have been reported t
82 ed with enhanced primary immune responses to allergic sensitization and elevated production of multip
83 SLP) and 2p23 (CAPN14), indicating roles for allergic sensitization and esophageal specific protease
84 , sociodemographic, and regional patterns of allergic sensitization and examined risk factors associa
85                                              Allergic sensitization and filaggrin gene (FLG) variants
86 on of allergic comorbidities associated with allergic sensitization and FLG variants emphasize their
87 tence of allergic disorders is frequent, and allergic sensitization and FLG variants jointly increase
88 stigating the single and combined effects of allergic sensitization and FLG variants on the developme
89                              Associations of allergic sensitization and FLG variants with single and
90            In repeated measurement analyses, allergic sensitization and FLG variants, when analysed s
91                    At age 10 years, inhalant allergic sensitization and food-allergic sensitization w
92 esting, only the associations of GIMAP4 with allergic sensitization and GIMAP5 with asthma remained s
93 rough the oral route may contribute to child allergic sensitization and have important implications f
94 exposure to DEP and HDM together exacerbated allergic sensitization and induced key characteristics o
95 s and whether this induction could determine allergic sensitization and inflammation.
96 tions between prenatal exposures to POPs and allergic sensitization and lung function in 20-year-old
97 e cells and skin cells and protected against allergic sensitization and lung inflammation through the
98 nted allergic diseases in mice by increasing allergic sensitization and memory immune responses.
99 gens and endotoxin and to the development of allergic sensitization and recurrent wheeze assessed at
100 imuli are associated with the development of allergic sensitization and recurrent wheeze.
101 elationship between plasma levels of TSLP to allergic sensitization and recurrent wheezing was conduc
102                      The association between allergic sensitization and rhinitis was consistently str
103 ish introduction was associated with reduced allergic sensitization and rhinitis.
104  environment and is commonly associated with allergic sensitization and severe asthma in humans.
105 ether triclosan exposure was associated with allergic sensitization and symptoms in 10-year-old Norwe
106 f DNA-PK in DCs, attenuates the induction of allergic sensitization and Th2 immunity via a mechanism
107 in through a disrupted skin barrier leads to allergic sensitization and that early oral exposure to f
108 ith FcepsilonRI is primarily responsible for allergic sensitization and the inflammatory response, wh
109                      Therefore, because both allergic sensitization and viral and bacterial illnesses
110  of investigators include the development of allergic sensitization and wheezing respiratory tract il
111 ear whether progenitors are recruited during allergic sensitization and whether recruitment promotes
112 o determine the association between EDCs and allergic sensitization and whether this relationship dep
113 ween diesel exhaust particle (DEP) exposure, allergic sensitization, and childhood wheezing, although
114 llergenic trees, discuss factors pivotal for allergic sensitization, and describe the role of tree po
115 perimental model of atopic dermatitis, TEWL, allergic sensitization, and epidermal thickness were inc
116 rhinitis appears less likely to be driven by allergic sensitization, and may imply disease onset in u
117 s limits skin barrier dysfunction, cutaneous allergic sensitization, and proinflammatory cytokine pro
118 e over the first 3 years was associated with allergic sensitization, and sensitization at age 3 years
119 with current rhinitis among children without allergic sensitization (AOR = 6.76; 95% CI: 1.21-37.74),
120 ata on the effect of smoking on rhinitis and allergic sensitization are inconsistent.
121 n-based studies about the natural history of allergic sensitization are rare.
122                                     Multiple allergic sensitizations are common in persistent childho
123 bese mice showed increased susceptibility to allergic sensitization as compared to LFD animals.
124                         Specific patterns of allergic sensitization as well as quantification of the
125                             The relevance of allergic sensitization, as judged by titers of serum IgE
126                         Associations between allergic sensitization, asthma, and eczema were estimate
127 t 1 year of age were associated with reduced allergic sensitization at 1 (P = 0.03) and 2 (P = 0.02)
128 ed with respect to lung function outcomes or allergic sensitization at 18 to 19 years of age.
129 aternal concentrations of POPs and offspring allergic sensitization at 20 years of age.
130 e associated with airway obstruction but not allergic sensitization at 20 years of age.
131 ut was positively associated with asthma and allergic sensitization at 7 years.
132                     Risk for asthma, AD, and allergic sensitization at age 6-7 were estimated from lo
133 two methods for diagnosing inhalant and food allergic sensitization at the four age points was analyz
134         Here we analyze the skin microbiota, allergic sensitization (atopy), and immune function in a
135 lies and in a prospective Swedish asthma and allergic sensitization birth cohort.
136 that BCG vaccination did not protect against allergic sensitization but might have exerted a protecti
137 c rhinitis (rhinitis without sensitization), allergic sensitization but no rhinitis, or neither rhini
138 arly life plays a role in the development of allergic sensitization but not in the development of res
139 f genetic variants have been associated with allergic sensitization, but whether these are allergen s
140  time of bronchiolitis or the development of allergic sensitization by age 3 years are associated wit
141                 The increasing prevalence of allergic sensitization by age was explained by high inci
142  effects of triclosan or paraben exposure on allergic sensitization by sex observed in this study war
143 ent asthma and rhinitis), puberty status and allergic sensitization by specific serum antibodies (imm
144 rolled (n = 31) asthmatics were assessed for allergic sensitization by two microarray systems (Microt
145                                     Although allergic sensitization can be generated against various
146 onship and the plausible mechanisms by which allergic sensitization can lead to more severe HRV-induc
147        Taken together, our data suggest that allergic sensitization coincident with filarial infectio
148 ure to TRAP in middle age is associated with allergic sensitization, current asthma, and reduced lung
149                                              Allergic sensitization decreased with increasing age, bo
150 mokers with COPD (n = 77) were evaluated for allergic sensitization defined as a detectable specific
151                    The overall prevalence of allergic sensitization does not vary across US census re
152                                              Allergic sensitization early in life, early-life infecti
153 ation, and household income, were fitted for allergic sensitization (either skin prick test positivit
154 h cohort we investigated whether concomitant allergic sensitization enhances subsequent development o
155 riclosan concentrations were associated with allergic sensitization, especially inhalant and seasonal
156 luding a high degree of comorbid conditions, allergic sensitization, exacerbations, and very poorly c
157 cts with filarial infections, and coincident allergic sensitization (filarial [Fil](+)allergy [A](+))
158 atients' demographic and historical factors, allergic sensitization, fraction of exhaled nitric oxide
159 ith genome-wide significant association with allergic sensitization from three to ten, including SNPs
160 ne learning approach to longitudinal data on allergic sensitization from two independent unselected b
161 onversely, persistence is linked strongly to allergic sensitization, greater frequency and severity o
162                        Atopic dermatitis and allergic sensitization had significant interactions on b
163        In combination, atopic dermatitis and allergic sensitization had strong interactive effects on
164                  Molecule-based profiling of allergic sensitization has helped to elucidate the immun
165 lergen-specific immunoglobulin E (present in allergic sensitization) has a central role in the pathog
166 f hay fever, eczema and objective markers of allergic sensitization have been found fairly consistent
167 oms, but associations with lung function and allergic sensitization have been minimally explored.
168  development of diisocyanate (dNCO)-specific allergic sensitization; however, MDI-haptenated albumins
169 did not lead to increased risk of subsequent allergic sensitization (HR, 0.76; 95% CI, 0.50-1.1).
170 cale genome-wide association study (GWAS) of allergic sensitization in 5,789 affected individuals and
171 et v 1-specific CD4(+) T cells and prevented allergic sensitization in a mouse allergy model.
172 ted fatty acids (n-3 LCPUFA) largely prevent allergic sensitization in a murine model for cow's milk
173 thyl phthalate was inversely associated with allergic sensitization in adults (OR = 0.79; 95% CI: 0.7
174 e exposures) were positively associated with allergic sensitization in adults.
175 ssociated with asthma at age 7 but not AD or allergic sensitization in at-risk children born at term.
176 , airway epithelial NF-kB activation induced allergic sensitization in CAIKKbeta mice on Dox that req
177 posure is associated with the development of allergic sensitization in childhood as reflected by glob
178 S exposure contributes to the development of allergic sensitization in children and adolescents up to
179  smoke (SHS) exposure and the development of allergic sensitization in children is unclear.
180 en air pollution exposure and development of allergic sensitization in children up to 10 years of age
181 oncurrent asthma, altered lung function, and allergic sensitization in children.
182 both asthma inception and exacerbations, and allergic sensitization in early life further enhances as
183 sly showed that the ability of HDM to induce allergic sensitization in mice is related to airway epit
184 hosphate (ATP)-dependent Ca(2+) signaling in allergic sensitization in mice, we sought to determine t
185 n linked to both induction and protection of allergic sensitization in offspring.
186                                  We compared allergic sensitization in patients with food allergy or
187 , remission, risk factors, and prevalence of allergic sensitization in relation to aging over a 10-ye
188           Elevated hs-CRP is associated with allergic sensitization in school-aged children suggestin
189 s and childhood asthma, recurrent wheeze, or allergic sensitization in the overall study population.
190                  The development of specific allergic sensitization in the skin of those patients fol
191 ve interaction between atopic dermatitis and allergic sensitization in their effects on food allergy
192 piratory illnesses support a causal role for allergic sensitization in this developmental pathway.
193 greement between SPT and sIgE for diagnosing allergic sensitization in young children, which increase
194           Conversely, atopic dermatitis with allergic sensitization increased the risk of asthma more
195 atures with the exception of some markers of allergic sensitization, indicating a need to develop bet
196 d pollen-intrinsic NADPH oxidase activity in allergic sensitization, inflammation, and airway hyperre
197 associations of breastfeeding with childhood allergic sensitization, inhalant or food allergy and ecz
198 he link between skin barrier dysfunction and allergic sensitization initiating the atopic march.
199                                              Allergic sensitization is a multifactorial process that
200                                              Allergic sensitization is a particularly difficult proce
201                                              Allergic sensitization is an important risk factor for t
202 hanism underlying clinical observations that allergic sensitization is associated with increased susc
203  is widely distributed in homes and schools; allergic sensitization is common.
204                                              Allergic sensitization is initiated by allergen-specific
205 hibitory effect of uricase administration on allergic sensitization is mediated more through Ag-speci
206 ests when the identification of the specific allergic sensitization is required for patient managemen
207 sensitization on allergic multimorbidity and allergic sensitization is unclear.
208 ous metabolite 9-cis retinoic acid (9cRA) on allergic sensitization is unknown.
209 s a critical role in the induction of peanut-allergic sensitization, likely due to its ability to act
210       Associations between TRAP exposure and allergic sensitization, lung function, current wheeze, a
211  Therefore, therapeutics aimed at preventing allergic sensitization may modify virus-induced wheezing
212                 MBzP was not associated with allergic sensitization, nor did seroatopy modify consist
213 ients is consistent with the hypothesis that allergic sensitization occurs through the skin.
214 5571 was associated with risk for asthma and allergic sensitization (odds ratio [OR] 3.74, p = 0.0007
215 somal phenotype was related to lifestyle and allergic sensitization of the mothers, and sensitization
216 ght present a critical period for preventing allergic sensitization of the progeny.
217 aracteristics were not related to subsequent allergic sensitization or disease.
218 ly nonmodifiable factors, particularly early allergic sensitization or eczema and parental AR, predic
219                                         Once allergic sensitization or eczema is established, CD4(+)C
220 eak overall increased risk of eczema but not allergic sensitization or physician-diagnosed allergy at
221 ne whether there are differences in rates of allergic sensitization or prior diagnoses of asthma, hay
222 osure does not seem to affect development of allergic sensitization or rhinitis during childhood ques
223 ociated with asthma (OR 1.28, p = 0.035) and allergic sensitization (OR 1.27, p = 0.0068).
224 ce interval (CI): 0.61, 0.76; P < 0.001) and allergic sensitization (OR = 0.74, 95% CI: 0.64, 0.86; P
225 I: 0.920, 0.998; P = 0.041), a lower risk of allergic sensitization (OR = 0.92, 95% CI: 0.84, 1.02; P
226  (OR = 1.10 [1.01-1.12], P = 0.033) and with allergic sensitization (OR = 1.10 [1.03-1.17], P = 0.003
227 y fever (OR= 0.998; 95% CI: 0.994, 1.002) or allergic sensitization (OR=0.999; 95% CI: 0.986, 1.012)
228  circulating TSLP is associated with eczema, allergic sensitization, or recurrent wheezing in young c
229 f CD4(+)CD25(+) FoxP3(+) T cell numbers with allergic sensitization (P = 0.05) and eczema (P = 0.02).
230 ved no association of breastfeeding with any allergic sensitization, physician-diagnosed allergy, or
231 rization of a birth cohort demonstrated that allergic sensitization precedes HRV wheezing and that th
232 airway disease but may be overcome to induce allergic sensitization preceding the development of asth
233 curred at Hokkaido University, we studied on allergic sensitization prevalence for laboratory animals
234  of the present study was to investigate the allergic sensitization profile in asthmatics and examine
235 alysing specific patterns of an individual's allergic sensitization profile reveals additional releva
236     The processes involved in the genesis of allergic sensitization remain elusive.
237 osure to air pollution in the development of allergic sensitization remains unclear.
238  birth to age 10 years and susceptibility to allergic sensitization, respiratory tract infections, an
239 inical examination including measurements of allergic sensitization (serum-specific IgE >/= 0.35 kUA
240 e causal effect of BMI on asthma, hay fever, allergic sensitization, serum total immunoglobulin E (Ig
241 ed the clusters in two models: age of onset, allergic sensitization, severity, and recent exacerbatio
242                                              Allergic sensitization showed no association with asthma
243  increased eosinophilic airway inflammation, allergic sensitization, TH2 cytokine production, and muc
244 ibutor to barrier disruption associated with allergic sensitization, there is a need to better unders
245  interdependency between asthma, eczema, and allergic sensitization through childhood.
246                                              Allergic sensitization through the airway primed both ef
247                            The prevalence of allergic sensitization to any aeroallergen was 51% (95%
248  MD2 plays an important role in induction of allergic sensitization to cat dander and common pollens
249                                              Allergic sensitization to cat, dog, and house dust mites
250 sociation between air pollution exposure and allergic sensitization to common allergens in children f
251 ed OR = 4.4, 95% CI 1.5-13.7 for 2 parents); allergic sensitization to common household aeroallergens
252 ctors include elevated exhaled nitric oxide, allergic sensitization to common household aeroallergens
253 e 25% for high exhaled nitric oxide, 22% for allergic sensitization to common household aeroallergens
254  role of the AD skin phenotype in modulating allergic sensitization to common sensitizers has not bee
255 h2 effector cell differentiation and prevent allergic sensitization to dietary antigens.
256 ion of Th2 effector cell differentiation and allergic sensitization to dietary antigens.
257         Birth cohort studies have shown that allergic sensitization to food allergens develops early
258  behind the induction of T(H)2 responses and allergic sensitization to food antigens largely remains
259 n-diagnosed asthma or recurrent wheezing and allergic sensitization to food or environmental antigens
260 ively breastfed children, this suggests that allergic sensitization to foods can be mediated by cutan
261 ation of the immunologic pathways underlying allergic sensitization to foods in humans has been great
262 n essential requisite for the development of allergic sensitization to foods.
263 arrier impairment, and AD also predispose to allergic sensitization to foods.
264                                              Allergic sensitization to fungi has been associated with
265 ollen allergens that are thought to initiate allergic sensitization to grass pollen.
266                                Consequently, allergic sensitization to HDM was abolished in vivo when
267 uggests they might promote asthma by priming allergic sensitization to inhaled allergens.
268                                              Allergic sensitization to inhaled antigens is common but
269 ctions with pneumonia virus of mice promoted allergic sensitization to inhaled cockroach antigen in t
270 g dendritic cells (DCs) in vitro and promote allergic sensitization to inhaled innocuous proteins in
271                            Susceptibility to allergic sensitization to mite allergens in mice was hig
272 nd the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple foods.
273 ss, lung resistance, and TH2 responses after allergic sensitization to ovalbumin.
274  to structurally intact skin did not lead to allergic sensitization to peanut or OVA.
275 tors critically involved in the induction of allergic sensitization to peanut.
276 h breast milk may prevent instead of priming allergic sensitization to peanut.
277 oxidative stress plays a significant role in allergic sensitization to pollen via the airway mucosa,
278 P, highlighting an important role for SPP in allergic sensitization to short ragweed.
279 ized the main molecular pathways involved in allergic sensitization to subtilisin that potentially co
280 ess was associated with higher prevalence of allergic sensitization to tree pollen.
281 ze, eczema, allergic rhinitis, food allergy, allergic sensitization, type 1 diabetes mellitus, celiac
282 y through modulating susceptibility to early allergic sensitization, upper respiratory tract coloniza
283 erite children, the prevalence of asthma and allergic sensitization was 4 and 6 times as low in the A
284              The role of oxidative stress in allergic sensitization was also investigated in humans.
285                                          The allergic sensitization was determined based on skin pric
286                                              Allergic sensitization was determined by skin prick test
287 gh-affinity IgE Fc receptor (FcepsilonRI) in allergic sensitization was evaluated using Was(-/-) Fcer
288                    Atopic dermatitis without allergic sensitization was not associated with an increa
289        Atopic dermatitis without concomitant allergic sensitization was not associated with an increa
290                                              Allergic sensitization was not significantly associated
291                         A high prevalence of allergic sensitization was observed in this cohort.
292 n between triclosan and paraben exposure and allergic sensitization was observed.
293 pic evaluation of allergic rhinitis (AR) and allergic sensitization was performed on 2153 children fr
294 esophageal expression, and multiple loci for allergic sensitization were associated with EoE suscepti
295 bo/control, for treating AE in patients with allergic sensitization were eligible.
296 d reported allergic or autoimmune disease or allergic sensitization were included.
297 rs, inhalant allergic sensitization and food-allergic sensitization were measured by skin prick tests
298                    The main risk factors for allergic sensitization were young age and a family histo
299  findings will have a major influence on how allergic sensitization will be viewed and studied in the
300 nature of EoE that involves the interplay of allergic sensitization with an EoE-specific, IL-13-induc

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