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1 PIES) is a non-IgE-mediated gastrointestinal allergic disorder.
2 20% of the global population suffers from an allergic disorder.
3 nd survey its clinical efficacy in different allergic disorders.
4 n be used to analyze complex respiratory and allergic disorders.
5 nd their association with the development of allergic disorders.
6 harbors helminth infections or suffers from allergic disorders.
7 ent of novel approaches for the treatment of allergic disorders.
8 pathogenesis of infectious, autoimmune, and allergic disorders.
9 rtant in the pathogenesis of anaphylaxis and allergic disorders.
10 ssue resident cells with a principal role in allergic disorders.
11 e adaptive immune response that causes these allergic disorders.
12 particles (DEP), promotes the development of allergic disorders.
13 onic inflammation associated with asthma and allergic disorders.
14 y responses associated with asthma and other allergic disorders.
15 innate immunity and regulation of autoimmune/allergic disorders.
16 inking their possible roles with exacerbated allergic disorders.
17 ternal-fetal interactions may occur in other allergic disorders.
18 osed as one mechanism to explain the rise in allergic disorders.
19 ical target for the regulation of autoimmune/allergic disorders.
20 of cytokines and chemokines associated with allergic disorders.
21 fundamentally new concept for the control of allergic disorders.
22 cologically targeting arginine metabolism in allergic disorders.
23 eosinophils in a variety of inflammatory or allergic disorders.
24 develop safe immunotherapeutic strategy for allergic disorders.
25 to the eosinophilia seen in asthma and other allergic disorders.
26 d implicated as a genetic predisposition for allergic disorders.
27 T cell heterogeneity is highly relevant to allergic disorders.
28 also be elevated in individuals with severe allergic disorders.
29 hn's disease and rheumatoid arthritis and in allergic disorders.
30 rovide a novel strategy for the treatment of allergic disorders.
31 tality associated with anaphylaxis and other allergic disorders.
32 extracellular mediators of inflammation and allergic disorders.
33 oimmunity, autoinflammation, malignancy, and allergic disorders.
34 rease the susceptibility to inflammatory and allergic disorders.
35 pathways underlying the pathogenesis of food-allergic disorders.
36 is the only disease-modifying treatment for allergic disorders.
37 acute and life-threatening manifestation of allergic disorders.
38 to describe the group of heritable monogenic allergic disorders.
39 that develops several years after preceding allergic disorders.
40 efficient and cost-effective method to treat allergic disorders.
41 ith monocyte and macrophage responses across allergic disorders.
42 to the inflammation of other non-respiratory allergic disorders.
43 markedly reduced the public health burden of allergic disorders.
44 system development and decrease the risk of allergic disorders.
45 sents the typical trajectory associated with allergic disorders.
46 me pathologic in the setting of a variety of allergic disorders.
47 r chronic itch in the setting of a number of allergic disorders.
48 e pro-inflammatory responses associated with allergic disorders.
49 iated with risk of childhood asthma or other allergic disorders.
50 an interesting approach for the treatment of allergic disorders.
51 to an even broader list of hypersensitivity/allergic disorders.
52 for the design of novel immunotherapies for allergic disorders.
53 of the IL-21/IL-21R system in the context of allergic disorders.
54 classes of fatigue, sleep disturbances, and allergic disorders.
55 al integrity, such as acute inflammatory and allergic disorders.
56 ls are frequently increased in patients with allergic disorders.
57 tecting pollen allergens as measures against allergic disorders.
58 as well as in autoimmune, inflammatory, and allergic disorders.
59 ential adjuvants for FcepsilonRI-MC-mediated allergic disorders.
60 Biologicals have also been tested in allergic disorders.
61 ould be exploited for the treatment of human allergic disorders.
62 ir detrimental contributions to IgE-mediated allergic disorders.
63 to transform the diagnosis and treatment of allergic disorders.
64 may affect the initiation and maintenance of allergic disorders.
65 e associated with having single and multiple allergic disorders.
66 ave recently been shown to play key roles in allergic disorders.
67 ts on the development of single and multiple allergic disorders.
68 lturally applicable classification system of allergic disorders.
69 heir joint importance in the pathogenesis of allergic disorders.
70 allergic asthma and other mast cell-mediated allergic disorders.
71 ratory disorders, such as asthma and related allergic disorders.
72 with play a key role in the pathogenesis of allergic disorders.
73 the only causative treatment of IgE-mediated allergic disorders.
74 preventative and therapeutic strategies for allergic disorders.
75 that manifest clinically as asthma and other allergic disorders.
76 significantly higher odds of developing any allergic disorders (adjusted OR, 3.04; 95% CI, 1.08-8.60
77 apacity of pDCs in patients with one type of allergic disorder, allergic asthma, and controls; 2) to
78 significantly advanced our understanding of allergic disorders, allowing scientists and clinicians t
79 onsequences, including an increased risk for allergic disorders and asthma later in childhood, the me
83 olvement of cytokines and other mediators in allergic disorders and described novel approaches for un
84 ely recognized as critical effector cells in allergic disorders and other immunoglobulin E-associated
86 lated goals of preventing the development of allergic disorders and providing the most effective diag
87 elopmental contribution to the risk of later allergic disorders and suggest that involvement of epige
88 ood therapy, novel diagnostics in diagnosing allergic disorders and the central role that omics play
90 uction and treatment of autoimmune diseases, allergic disorders, and graft rejection by depleting und
95 actions underlying the early-life origins of allergic disorders, as well as immune mechanisms that mi
96 ulatory cells in immunoglobulin E-associated allergic disorders, as well as in certain innate and ada
98 min D may be involved in the pathogenesis of allergic disorders, asthma and decreased lung function.
99 on in early childhood and atopy and reported allergic disorders at the age of 6.5 years in an Ethiopi
100 from 2008 to 2018 to mitigate the burden of allergic disorders by revisiting the prevention strategy
105 ed of health professionals' attitudes toward allergic disorders classification supports the need to u
106 mplification process of the hypersensitivity/allergic disorders classification was carried out to bet
107 f healthcare professionals' attitudes toward allergic disorders classification was proposed to the me
112 review summarizes work using BTKis to treat allergic disorders, emphasizing safety and practical con
113 and possibly other Ab-mediated autoimmune or allergic disorders, especially when given in short cours
115 urticaria, venom allergy and other probable allergic disorders) from the Scottish Primary Care Clini
116 cable disease outcomes, including asthma and allergic disorders, growth and development, cardio-metab
117 iologic mechanisms underlying IgE-associated allergic disorders has led to the identification of nove
118 pothesis that IgE, which also contributes to allergic disorders, has an important function in protect
119 responsiveness, revealing that patients with allergic disorders have an increased nasal mucosal IFN a
122 FLG) variants are important risk factors for allergic disorders; however, knowledge on their individu
123 correlates with a reduced risk of atopy and allergic disorders; however, limited data are available
124 the pathophysiology of bronchial asthma and allergic disorders; however, this concept was challenged
125 roteins in IgE-based serologic assessment of allergic disorders in a helminth-infected population, we
127 associated with the development of multiple allergic disorders in humans, indicating that TSLP is a
128 se dust mite-derived proteases contribute to allergic disorders in part by disrupting epithelial barr
129 or autoimmune, infectious, inflammatory, and allergic disorders in the etiology of multiple myeloma (
130 ve useful in the treatment of autoimmune and allergic disorders in which iNKT cell activation is dest
132 genes that contribute to the development of allergic disorders include leukocyte histocompatibility
133 s play an important role in eliciting type 1 allergic disorders including asthma and allergic rhiniti
136 been implicated by their presence in diverse allergic disorders including bronchial asthma, allergic
138 aureus, a major human pathogen, exacerbates allergic disorders, including atopic dermatitis, nasal p
139 s are also implicated in the pathogenesis of allergic disorders, including eosinophilic esophagitis (
140 e so inextricably linked to the pathology of allergic disorders, including fatal anaphylaxis, that it
145 presented whereby the evolution of specific allergic disorders is predicated on the confluence of pr
146 The role of T(H) in autoimmune-disorders and allergic-disorders is now re-evaluated, with current dat
147 ly in the context of lung- and skin-specific allergic disorders, it is becoming increasingly clear th
148 le of mast cells, critical effector cells in allergic disorders, known to interact with ILC2s in vivo
149 e of the IgE response in the pathogenesis of allergic disorders, little is known about the role of fo
150 eir historical role as the effector cells in allergic disorders, mast cells have been implicated in r
151 the presence of degranulated MC in various (allergic) disorders, MC-derived EV should be considered
152 evalence and incidence of atopy and reported allergic disorders (measured at age of 6.5 years) were d
154 C) are well known for their effector role in allergic disorders; moreover, they are associated with d
155 n-IgE-mediated gastrointestinal food-induced allergic disorders (non-IgE-GI-FAs) account for an unkno
156 n the brain, heart, synovium and intestines, allergic disorders of the lung and skin, and microbial i
159 acterize their effects on the development of allergic disorders on the basis of available literature
160 oduction leads to epidermal and consequently allergic disorders, our findings emphasize the need for
161 CF or anti-Kit antibodies in mouse models of allergic disorders, parasite immunity, or fibrosis in wh
162 Complex pathogenetic pathways observed in allergic disorders present a challenge in patient manage
163 food allergy encompasses a wide spectrum of allergic disorders ranging from mild to severe presentat
167 iencies, autoimmune disorders, and even some allergic disorders share overlapping autoinflammatory fe
168 iew, we suggest that these endotypes of food-allergic disorders should be defined on the basis of (1)
177 hought to be critical to the pathogenesis of allergic disorders, such as anaphylaxis and asthma, and
178 tical role in the pathology of IgE-dependent allergic disorders, such as anaphylaxis and asthma.
180 proinflammatory mediators that contribute to allergic disorders, such as asthma and anaphylaxis.
181 itors are also effective in the treatment of allergic disorders, such as atopic dermatitis, and can e
182 otic syndrome (MCNS), which often complicate allergic disorders that show a similar helper T-cell pro
183 to the proinflammatory role of mast cells in allergic disorders, the results obtained in this study e
184 of the GSTP1 gene may influence the risk for allergic disorders through an impaired defence against o
186 athway has been previously linked to various allergic disorders, we provide unexpected evidence for i
187 or metabolic, respiratory, neurological, and allergic disorders were substantially increased in child
188 on and FLG variants with single and multiple allergic disorders were tested in log-binomial regressio
189 implicated in inflammatory conditions beyond allergic disorders where IgE-mediated facilitated antige
190 worm burden tended to have increased risk of allergic disorder, whereas low IgE/high worm burden tend
191 pted to be an antigen-driven, TH2-associated allergic disorder, whereas the cause of PPI-REE remains
192 ver of type 1 hypersensitivity reactions and allergic disorders, which are globally increasing in num
193 lic esophagitis (EoE), a recently recognized allergic disorder with poorly understood pathogenesis.
194 ed a common molecular signature across major allergic disorders, with consistent enrichment in interl