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1 driver of type2/Th2 immune diseases (atopic/allergic diseases).
2 tiology of type 2 CD4(+) T cell responses in allergic disease.
3 rch and further progression of this systemic allergic disease.
4 work synergistically to control IgE-mediated allergic disease.
5 is a key priority for reducing the burden of allergic disease.
6 ed in human infants, before their developing allergic disease.
7 ve stress in models of adolescent asthma and allergic disease.
8 duction in the incidence of some symptoms of allergic disease.
9 ty can be associated with the development of allergic disease.
10 on at birth have been linked with subsequent allergic disease.
11 microbiome and influence the development of allergic disease.
12 d have implications for our understanding of allergic disease.
13 sensitization and subsequent development of allergic disease.
14 therapeutic strategies to treat and prevent allergic disease.
15 ontact hypersensitivity (CHS), a common skin allergic disease.
16 might be critical for preventing asthma and allergic disease.
17 hat might play a role in human infections or allergic disease.
18 ese molecules in immunological mechanisms of allergic disease.
19 promise for the prevention and treatment of allergic disease.
20 tory taxa could be studied for prevention of allergic disease.
21 t type 2 inflammation can cause debilitating allergic disease.
22 genera in children developing IgE-associated allergic disease.
23 have been few studies on antibiotic use and allergic disease.
24 ing, and still there is a high prevalence of allergic disease.
25 ng use of anti-IgE mAbs for the treatment of allergic disease.
26 the potential to alter the natural course of allergic disease.
27 he type 2 immune responses that characterize allergic disease.
28 ch is the primary causal factor in childhood allergic disease.
29 uents and proteases, causing or exacerbating allergic disease.
30 ct against egg allergy in infants at risk of allergic disease.
31 hildhood may contribute to the prevention of allergic disease.
32 e dose in the prevention of autoimmunity and allergic disease.
33 the origin of the various manifestations of allergic disease.
34 ly sialylation, as an important regulator of allergic disease.
35 al distress increases the risk for childhood allergic disease.
36 3, but not IL25 or TSLP or other features of allergic disease.
37 iagnosis, management, and prevention of this allergic disease.
38 lead to immunodeficiency and, paradoxically, allergic disease.
39 st way to treat complex patients with severe allergic disease.
40 to antigen-specific vertical transmission of allergic disease.
41 e sclerosis, inflammatory bowel disease, and allergic disease.
42 anaphylaxis in several functional models of allergic disease.
43 rgeting type 2 inflammation in patients with allergic disease.
44 arget mast cells during anaphylaxis or other allergic diseases.
45 potentially be used in a broader spectrum of allergic diseases.
46 primary tool for diagnosis and treatment of allergic diseases.
47 mitations, and risks of mobile solutions for allergic diseases.
48 en linked to an increased risk of asthma and allergic diseases.
49 disease mechanisms to optimize management of allergic diseases.
50 hether cheese consumption is associated with allergic diseases.
51 translational relevance to the treatment of allergic diseases.
52 o promote the development and progression of allergic diseases.
53 T(H)2-driven inflammation, which relates to allergic diseases.
54 on, including in the treatment of cancer and allergic diseases.
55 cepsilonRI), which play an essential role in allergic diseases.
56 etence and contribute to the pathogenesis of allergic diseases.
57 ontent in drinking water may protect against allergic diseases.
58 idence but that effects might differ between allergic diseases.
59 investigate the terms reflecting pollen and allergic diseases.
60 have been widely investigated in asthma and allergic diseases.
61 gering or protecting against the onset of GI allergic diseases.
62 t cell populations and mechanisms underlying allergic diseases.
63 , and aetiological origins of autoimmune and allergic diseases.
64 e development and exacerbation of asthma and allergic diseases.
65 l age in relation to onset of IgE-associated allergic diseases.
66 garding the relevance of anti-glycan IgE for allergic diseases.
67 tic purposes or therapeutic interventions of allergic diseases.
68 target for EoE and related eosinophilic and allergic diseases.
69 e PUFAs may be important in the aetiology of allergic diseases.
70 associated immune responses in patients with allergic diseases.
71 to be used for the prevention of asthma and allergic diseases.
72 be used to report the seasonal variations of allergic diseases.
73 responsible for the increasing prevalence of allergic diseases.
74 ne disorders, cancer, and cardiovascular and allergic diseases.
75 reventative, and participatory approaches in allergic diseases.
76 evising appropriately targeted therapies for allergic diseases.
77 reatment of infections and cancer as well as allergic diseases.
78 tween atopic dermatitis phenotypes and other allergic diseases.
79 of immune tolerance, becomes insufficient in allergic diseases.
80 17-producing T cells have important roles in allergic diseases.
81 lls that may be harnessed for the control of allergic diseases.
82 rise as a new target for the manipulation of allergic diseases.
83 re common among some congenital and acquired allergic diseases.
84 IgE is a therapeutic target in patients with allergic diseases.
85 fatty acids influence the risk of childhood allergic diseases.
86 entially more efficient way of treatment for allergic diseases.
87 ches to the blockade of pathways involved in allergic diseases.
88 (Treg) play an important role in preventing allergic diseases.
89 otal cytokines involved in the generation of allergic diseases.
90 some of the protective effects of TB against allergic diseases.
91 antibody isotype in TH2-biased immunity and allergic diseases.
92 is targeted to modify the natural history of allergic diseases.
93 moral factors such as IgE are key drivers of allergic diseases.
94 have been associated with increased rate of allergic diseases.
95 e service for the diagnosis and treatment of allergic diseases.
96 hat might exist for early-life prevention of allergic diseases.
97 s [2.62 (1.79-3.83)] and mother's history of allergic disease [2.12 (1.48-3.02)]; frequent de-worming
99 for their detrimental role in patients with allergic diseases, act in a diverse array of physiologic
100 lt-onset asthma increased with the number of allergic diseases; adjusted OR for asthma [95% CI] assoc
102 developments in the three prototype chronic allergic diseases allergic asthma, chronic spontaneous u
103 pulation-based cohort, the prevalence of any allergic disease among 4-year-old children in Melbourne,
104 children were diagnosed with IgE-associated allergic disease and 90% displayed allergic comorbidity.
106 9 associated genes to the pathophysiology of allergic disease and assess their therapeutic potential
107 is HMOs was associated with a higher risk of allergic disease and asthma over childhood (odds ratio a
108 nterested in the effects of air pollution on allergic disease and asthma should carefully consider th
109 portant knowledge gaps regarding its role in allergic disease and delineating strategies necessary to
110 nosuppression and infectious mononucleosis), allergic disease and eczema are risk factors for HL.
111 ntrol, psychosocial issues, adolescent-onset allergic disease and female sex; (b) Psychological facto
113 Westernized populations have high rates of allergic disease and low rates of gastrointestinal carri
114 UFA levels in colostrum and breast milk with allergic disease and lung function at ages 12 and 18 yea
115 onical type 2 cytokine IL-4, which underpins allergic disease and parasitic worm infections, than mac
116 hes to exposome modification in AD and other allergic disease and propose future directions for expos
118 baseline to estimate their association with allergic diseases and asthma at the ages of 4 and 7.
121 e essential to ensure a better management of allergic diseases and asthma in the advent of precision
122 ing, big data and information technology and allergic diseases and asthma in the context of environme
128 odies are best known for pathogenic roles in allergic diseases and for protective effector functions
129 childhood and examine their association with allergic diseases and hereditary background in Finland a
130 regression investigated associations between allergic diseases and HL after adjusting for established
131 cular and cellular mechanisms that govern GI allergic diseases and how these findings have set the st
132 t option in almost two-third of all types of allergic diseases and in 90% of individuals suffering fr
133 s first option in almost 2/3 of all types of allergic diseases and in 90% regarding respiratory aller
134 ys are most important in the pathogenesis of allergic diseases and in the development of symptoms and
135 rch shows an association between the rise of allergic diseases and increasingly modern Westernized li
138 have been shown to affect the development of allergic diseases and the recent developments in the fie
139 o their importance in the pathophysiology of allergic diseases and their potential as biomarkers in l
140 long implicated in antiparasite immunity and allergic diseases and, more recently, in regulating adip
141 d associations between n-3 and n-6 PUFAs and allergic disease, and the magnitude of this effect varie
143 was positively associated with the number of allergic diseases, and this association decreases with a
144 alk has a key role in the pathophysiology of allergic diseases, and we present evidence indicating th
146 that allergy evolved for a purpose and that allergic diseases are accidental consequences of an insu
147 nsitization and high frequencies of comorbid allergic diseases are characteristic of severe asthma in
148 ing susceptibility to complex autoimmune and allergic diseases are concentrated within noncoding regu
150 r, clinical studies with bacteria to prevent allergic diseases are still rare and to some extent cont
154 mechanisms that underlie the development of allergic disease, as well as the processes that drive im
155 phagitis (EoE) is an emerging, chronic, rare allergic disease associated with marked eosinophil accum
156 Eosinophilic esophagitis (EoE) is a chronic allergic disease associated with marked mucosal eosinoph
157 merged as an explanation for higher rates of allergic diseases associated with industrialization and
159 ght to assess the risk of HL associated with allergic disease (asthma, eczema, and allergic rhinitis)
160 s defined as having symptoms from at least 1 allergic disease (asthma, rhinitis, or eczema) and posit
164 isease, including cardiometabolic disorders, allergic diseases, autoimmune disorders, infections, and
167 apeutic target in patients with IgE-mediated allergic diseases because it seems to be involved in the
168 ofound complexity and dynamic variability in allergic disease between individuals, as well as between
171 nfants born preterm are at increased risk of allergic disease, but it is unknown if DHA supplementati
172 biota have been implicated in IgE-associated allergic diseases, but there is lack of longitudinal stu
175 ared with other defined groups of asthma and allergic disease cases; adult-onset asthma and moderate-
178 re administered in vivo in a mouse model for allergic disease (daily for 3-11 days, n = 5) and employ
179 In the quantitative analysis, the risk of allergic diseases decreased significantly with increasin
186 ymptom, suggesting that commonly encountered allergic diseases exist on a spectrum of monogenic and c
187 onable efficacy of the current management of allergic diseases facilitated the emergence of the endot
188 introduction of peanut on the development of allergic disease, food sensitization, and aeroallergen s
190 known function that is directly relevant to allergic disease: FOSL2, VPRBP, IPCEF1, PRR5L, NCF4, APO
191 e high prevalence and considerable impact of allergic disease globally, there needs to be a focus on
192 ity of biologic agents for the management of allergic diseases has been facilitated by recent advance
194 personalized allergen-specific management of allergic diseases has particularly contributed to early
195 he associations between breast milk PUFA and allergic disease have not previously been systematically
197 The prevalence, severity and complexity of allergic diseases have been increasing steadily in the U
200 formation was collected on family history of allergic diseases, household size, socioeconomic status,
201 hypothesized to influence the development of allergic diseases; however, few prospective studies have
202 at they might play a role in respiratory and allergic diseases; however, studies exploring these asso
204 t probiotics are effective for prevention of allergic disease in premature infants remains lacking; a
205 tion-based cohort experienced symptoms of an allergic disease in the first 4 years of their life.
206 damp indoor environments is associated with allergic disease in young children, but it is unclear wh
209 auterine growth restriction protects against allergic diseases in human subjects consistent with prec
210 n challenge-confirmed food allergy and other allergic diseases in preschool-aged children remain spar
211 acilitate clinical decision-making regarding allergic diseases in the context of hematopoietic stem c
212 tween environmental and dietary factors with allergic diseases in urban and rural South African child
215 a role in the development and progression of allergic disease, in particular allergic respiratory dis
216 m-born infants has been suggested to prevent allergic disease, in particular eczema; however, no stud
217 in patients with childhood-onset asthma and allergic diseases, in these important populations that c
219 holds that resistance to the development of allergic diseases, including allergic rhinoconjunctiviti
220 verview of the current research on miRNAs in allergic diseases, including atopic dermatitis, allergic
222 dysfunction is a significant factor in many allergic diseases, including eosinophilic esophagitis (E
223 licated in the development and regulation of allergic disease independent of their antibody reactivit
226 ly assumed that the contribution of fungi to allergic disease is mediated through their potent antige
229 ing in the development of oral tolerance and allergic diseases is controversial, which could be relat
234 In industrialized societies the incidence of allergic diseases like atopic dermatitis, food allergies
237 with a reduced incidence of inflammatory and allergic diseases.METHODSWe investigated the impact of B
238 e Keystone Symposium conference, "Origins of allergic disease: Microbial, epithelial and immune inter
240 intestinal microbiota and the development of allergic disease or asthma is less consistent in older c
242 vidence that immune system malfunction after allergic disease or immunosuppression is central to HL d
243 a probiotic combination on the incidence of allergic diseases or atopic sensitization in the first 2
246 nt in the lung tissue not only in pathology (allergic disease, parasite expulsion) but also during no
248 gnificant genetic overlap between asthma and allergic diseases, particularly with respect to childhoo
249 pments that have generated new insights into allergic disease pathogenesis, and how these could poten
250 ether the effects of prenatal growth on each allergic disease persist or differ between those with se
254 rts in basic science and clinical aspects of allergic diseases provided substantial insight into the
255 de association studies (GWASs) of asthma and allergic diseases published between January 1, 2018, and
256 fective prevention and treatment of epidemic allergic diseases remain limited, and particularly so fo
257 y more risk loci shared between these common allergic diseases remain to be discovered, which could p
259 e, we show that the prominent autoimmune and allergic disease risk locus at chromosome 11q13.5(2-7) c
263 ommend that infants of any risk category for allergic disease should have a diverse diet, given no ev
264 is a well-established protective factor for allergic disease, strongly predicts maternal carriage of
267 ggrin gene are a significant risk factor for allergic diseases such as atopic dermatitis, asthma, all
273 he incidence and severity of parent-reported allergic disease symptoms at a corrected age (CA) of 7 y
274 Parent-reported incidence of respiratory allergic disease symptoms including wheeze and rhinitis
275 fants born at <33 wk gestation did not alter allergic disease symptoms or severity at 7 y CA, or from
278 sed approach, we identified 11 risk loci for allergic disease that were not reported in previous GWAS
287 allergen and aeroallergen sensitization and allergic disease was noted across study time points; 76%
288 asthma [95% CI] associated with 1, 2, and 3 allergic diseases was 1.95 [1.52-2.49], 2.87 [2.19-3.77]
289 ctive effect of early food diversity against allergic diseases was previously shown in the PASTURE co
290 0-0]; P < .0001), and lifetime prevalence of allergic diseases was significantly lower among children
291 methylation at birth and the development of allergic disease, we examined the methylation status of
292 cohort of children with a family history of allergic diseases, we modeled the association between cu
293 of parental clinical outcome with offspring allergic disease were estimated with multinomial logisti
294 eeding practices, environmental factors, and allergic diseases were collected by questionnaires from
296 ble remedies for treatment and prevention of allergic diseases were discussed, including a precision
297 nophilic esophagitis, a prototypic, chronic, allergic disease, which provided a unique opportunity to
298 ings from studies evaluating associations of allergic disease with child behaviour require longitudin