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1 educe airway obstruction and inflammation in allergic asthma.
2 LS as a useful biomarker for moderate-severe allergic asthma.
3 ronchial biopsy specimens from patients with allergic asthma.
4 molecule could be a novel approach to treat allergic asthma.
5 the relevance of glycolysis in patients with allergic asthma.
6 ibody, is used to treat patients with severe allergic asthma.
7 ouse model of severe exacerbation of chronic allergic asthma.
8 f NSC23766 prevented AHR in murine models of allergic asthma.
9 Cs), which can be deficient in patients with allergic asthma.
10 f the enhanced susceptibility for TH2-driven allergic asthma.
11 onses and IgE formation in a murine model of allergic asthma.
12 or influenza infection on the development of allergic asthma.
13 is not known to modulate the pathogenesis of allergic asthma.
14 ddress its importance in the pathogenesis of allergic asthma.
15 through the skin and can provoke features of allergic asthma.
16 and eosinophilia) in a mouse model of severe allergic asthma.
17 agonists in mitigating multiple features of allergic asthma.
18 allergens are a common cause of allergy and allergic asthma.
19 iratory epithelia might provide insight into allergic asthma.
20 y trafficking of eosinophils in experimental allergic asthma.
21 igate its involvement in AHR associated with allergic asthma.
22 asis and initiate pathologic inflammation in allergic asthma.
23 LC2(10)s in the development and pathology of allergic asthma.
24 and is associated with allergic rhinitis and allergic asthma.
25 lso provide proof for a beneficial effect in allergic asthma.
26 ic target in the treatment and prevention of allergic asthma.
27 can be a risk factor for the development of allergic asthma.
28 ls in the regulation of hallmark features of allergic asthma.
29 ated influences on the overall prevalence of allergic asthma.
30 ergen-driven TH2 responses, promoting severe allergic asthma.
31 g alveolar macrophages suppressed HDM-driven allergic asthma.
32 may be a successful therapeutic strategy for allergic asthma.
33 f rhinovirus (RV) illnesses in children with allergic asthma.
34 .03); the opposite pattern was suggested for allergic asthma.
35 subjective burden of illness chain of severe allergic asthma.
36 brosis, maladaptive vascular remodeling, and allergic asthma.
37 t present important contributing features of allergic asthma.
38 tion in T cells from pediatric patients with allergic asthma.
39 reatment available for allergic rhinitis and allergic asthma.
40 il function and its role in a mouse model of allergic asthma.
41 mmunomodulatory approach to the treatment of allergic asthma.
42 ouse model of severe exacerbation of chronic allergic asthma.
43 +) T cells are critical for the induction of allergic asthma.
44 e assessed in a murine model of experimental allergic asthma.
45 and airways resistance in a murine model of allergic asthma.
46 helium-specific ERp57 in the pathogenesis of allergic asthma.
47 HDM) is a risk factor for the development of allergic asthma.
48 kin allergen responses in patients with mild allergic asthma.
49 nal role of 17q12-21 in patients with AR and allergic asthma.
50 jor signalling centre in the pathogenesis of allergic asthma.
51 ation, associated with poor lung function in allergic asthma.
52 late the cardinal clinical features of human allergic asthma.
53 tion of biomarkers for allergic rhinitis and allergic asthma.
54 B cells and Tfh cells in the pathogenesis of allergic asthma.
55 cepsilonRI expression in a clinical model of allergic asthma.
56 to allergens and is an important mediator of allergic asthma.
57 us) during the inception and exacerbation of allergic asthma.
58 kinase, may represent a novel treatment for allergic asthma.
59 n/interventional strategies for treatment of allergic asthma.
60 rgen-induced responses in subjects with mild allergic asthma.
61 s may be very effective for the treatment of allergic asthma.
62 erved in Citrobacter rodentium infection and allergic asthma.
63 erleukin 13, is used as treatment for severe allergic asthma.
64 ring the role of CD39 expression by Tregs in allergic asthma.
65 nd enhances susceptibility to a TH2 model of allergic asthma.
66 ically present in atopic diseases, including allergic asthma.
67 us production during house dust mite-induced allergic asthma.
68 crobiome for the treatment and prevention of allergic asthma.
69 verity among school children and adults with allergic asthma.
70 K may be a potential target for treatment of allergic asthma.
71 a significant cause of allergic rhinitis and allergic asthma.
72 can ameliorate inflammatory diseases such as allergic asthma.
73 after allergen provocation in patients with allergic asthma.
74 ons in circulating PBMCs are associated with allergic asthma.
75 l responses and promoting the development of allergic asthma.
76 te matter (PM) contribute to exacerbation of allergic asthma.
77 are the primary antigen-presenting cells in allergic asthma.
78 ns of vitamin E isoform gamma-tocotrienol in allergic asthma.
79 Tfh cells that results in protection against allergic asthma.
80 o mice with already established experimental allergic asthma.
81 therapeutic intervention for the control of allergic asthma.
82 cted against IgE can alleviate hay fever and allergic asthma.
83 ucocorticosteroid reduction in patients with allergic asthma.
84 IL-4 and IL-13 play a crucial role during allergic asthma.
85 the potential for Breg-targeted therapies in allergic asthma.
86 mechanisms of IT in a mouse model of chronic allergic asthma.
87 important for initiation and progression of allergic asthma.
88 ential to be used as a therapeutic option in allergic asthma.
89 LP) on Treg frequency using a human model of allergic asthma.
90 was sufficient to mediate protection against allergic asthma.
91 a promising new target for the treatment of allergic asthma.
92 nificant therapeutic benefit for T(H) 2-type allergic asthma.
93 r Be2 function was essential in experimental allergic asthma.
94 eted prevention and treatment strategies for allergic asthma.
95 ung neutrophils to promote the initiation of allergic asthma.
96 ipid metabolites as potential biomarkers for allergic asthma.
97 dance molecule b (RGMb), in murine models of allergic asthma.
98 ontribute to respiratory conditions, such as allergic asthma.
99 an innate RGMb-neogenin axis might modulate allergic asthma.
100 man eosinophil function and a mouse model of allergic asthma.
101 remains elusive, especially with respect to allergic asthma.
102 ould represent a novel therapeutic target in allergic asthma.
103 fat diet (HFD) feeding on the development of allergic asthma.
104 Only 2 studies reported allergic asthma.
105 faceted functions of ORMDL3 in patients with allergic asthma.
106 GG and L. rhamnosus GR-1 in a mouse model of allergic asthma.
107 oid cells (ILC2s) are important mediators of allergic asthma.
108 ndividuals or patients with allergic and non-allergic asthma.
109 chodilators, agents used in the treatment of allergic asthma.
110 o airway hyperreactivity in a mouse model of allergic asthma.
111 ole of ORMDL3 in sphingolipid metabolism and allergic asthma.
112 ht provide an important treatment option for allergic asthma.
113 sing a house dust mite (HDM) murine model of allergic asthma.
114 3-DMRs), environment IgE (17-CpGs; 4-DMRs), allergic asthma (1,235-CpGs; 7-DMRs) and bronchodilator
115 active COVID-19 infection in a patient with allergic asthma.(1) There are other emerging reports tha
116 have been identified include (1) early-onset allergic asthma, (2) early-onset allergic moderate-to-se
117 This effect appeared to be stronger for allergic asthma (22%; beta = 0.12; 95% CI: (-0.03, 0.27)
120 ide specific recommendations on treatment of allergic asthma (AA) caused by HDM allergy, although som
122 In the United States, the prevalence of allergic asthma (AA) is inexplicably rising and in utero
123 e treatment of moderate-to-severe persistent allergic asthma (AA) that remains uncontrolled despite h
126 cerbations) study, we examined children with allergic asthma (aged 6-17 yr; n = 478) from low-income
127 this study, we showed that the induction of allergic asthma alters the homeostasis of IL-10(+) Bregs
128 d for other T(H)2-mediated diseases, such as allergic asthma and atopic eczema, as well as purpose-de
130 in respiratory epithelia are associated with allergic asthma and gene expression changes in inner-cit
131 al cause of allergic rhinoconjunctivitis and allergic asthma and has the potential to alter the natur
132 ic rhinitis (AR), atopic dermatitis (AD) and allergic asthma and improved treatment options are neede
134 sinophils are critical cellular mediators in allergic asthma and inflammation; however, the signals t
135 tions can protect against the development of allergic asthma and might be further explored as a prote
136 tile targets for prevention or management of allergic asthma and other diseases in which adaptive imm
138 ent of AHR in the setting of DEP-exacerbated allergic asthma and reduced numbers of lung T(H)2/T(H)17
139 IL-4 receptor alpha (IL-4Ralpha) is key in allergic asthma and regulates type 2 cytokine production
140 ung, modestly CS-responsive individuals with allergic asthma and relatively normal lung function, sep
144 important source of indoor allergens causing allergic asthma and rhinitis in tropical and subtropical
146 Both allergen challenge in individuals with allergic asthma and the intranasal instillation of HDM i
147 h Factor Binding Proteins (IGFBPs)" route in allergic asthma and the lectin pathway of complement act
148 ether glycolysis is altered in patients with allergic asthma and to address its importance in the pat
149 sive panel of HDM allergens in children with allergic asthma and to compare them with those of nonast
150 he importance of PD-1 agonistic treatment in allergic asthma and underscore its therapeutic potential
151 tially regulated both in murine and in human allergic asthma and were associated with clinical charac
152 mouse model of house dust mite (HDM)-induced allergic asthma and whether it contributed to epithelial
153 (>/=12 years of age) with moderate to severe allergic asthma and who were being treated with omalizum
154 impairment, atopic dermatitis, food allergy, allergic asthma, and allergic rhinitis, it is logical th
155 luding food allergy (FA), allergic rhinitis, allergic asthma, and allergic rhinoconjunctivitis, a pro
156 represents a viable therapeutic strategy for allergic asthma, and strong TCR-mediated ERK activation
161 human nasal cells and used murine models of allergic asthma, as well as primary mouse tracheal epith
162 ases, including ischemia/reperfusion injury, allergic asthma, autoimmune nephritis, and rheumatoid ar
163 ed the following: (a) Biomarkers for AIT and allergic asthma; (b) visions for the future of AIT; (c)
165 alpha signaling on B cells is deleterious in allergic asthma because it is required for optimal T(H)2
168 d endotype, typically found in patients with allergic asthma, but surprisingly also in nonallergic pa
169 epresents an efficient strategy to alleviate allergic asthma, but the consequences of prolonged eosin
170 players in the induction and maintenance of allergic asthma by cross-linking innate and adaptive imm
171 ation of exogenous Sema3E protects mice from allergic asthma by reducing eosinophilic inflammation, s
172 ation was elicited in participants with mild allergic asthma by segmental allergen challenge before a
173 G-mediated cell signaling, protected against allergic asthma by simultaneously reducing airway inflam
177 he three prototype chronic allergic diseases allergic asthma, chronic spontaneous urticaria and atopi
178 rkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.
179 e existence of a new asthma phenotype (local allergic asthma) defined by absence of systemic atopy an
181 lly relevant asthma phenotypes: eosinophilic allergic asthma, eosinophilic nonallergic asthma and non
183 ti-IgE therapy that has improved outcomes in allergic asthma for more than a decade, three anti-IL-5
186 ertain gut microbiota and the development of allergic asthma has been shown in experiments conducted
187 owever, expression and function of Sema3E in allergic asthma has not been extensively investigated.
188 previously showed that patients with severe allergic asthma have high numbers of circulating ILC2s e
190 IT) for the management of allergic rhinitis, allergic asthma, IgE-mediated food allergy and venom all
193 ental influence on both epigenetic marks and allergic asthma in children, the epigenetic alterations
195 have recently been identified as inducers of allergic asthma in human subjects and mice, but their me
196 ells and their cytokines are associated with allergic asthma in human subjects and with mouse models
197 nic-cytidylic) acid exacerbated experimental allergic asthma in mice as characterized by enhanced rel
199 ex and weight gain alters the progression of allergic asthma in mice with females developing airway r
200 dy, we show that decreased responsiveness to allergic asthma in Pglyrp1 (-/-) mice (lacking bacterici
203 ntly inhibited all hallmarks of experimental allergic asthma, including airway hyperreactivity, eosin
204 er of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic
205 ate the expression of IL-31RA in vivo during allergic asthma induced by soluble egg antigen, which ma
207 ulating type 2 inflammation in patients with allergic asthma involving RGMb and RGMb-expressing cells
208 In contrast, deficiency of IL-13 prevented allergic asthma, irrespective of the presence or absence
236 oal was to delineate a mechanism(s) by which allergic asthma may alleviate influenza disease outcome,
237 viding a novel mechanism by which hosts with allergic asthma may be protected from influenza morbidit
238 erties of cysteinyl leukotrienes (cysLTs) in allergic asthma mediate their effects predominantly thro
239 ir proteins, and apoptosis in an HDM-induced allergic asthma model and in lung samples from asthmatic
241 prisingly, in contrast to our findings in an allergic asthma model, we found that the severity of hyp
243 recent evidence that SCFAs are beneficial in allergic asthma models, the effect on eosinophils has re
245 patients with persistent moderate-to-severe allergic asthma not sufficiently controlled on standard
246 fferences in the development and severity of allergic asthma observed between men and women of reprod
250 rgic rhinoconjunctivitis (PAR) and perennial allergic asthma (PAA) caused by indoor allergens in adul
251 notable contributions to chronic HDM-induced allergic asthma pathology by facilitating clustering and
252 d asthma control was particularly evident in allergic asthma patients and correlated with decreased f
254 , and remodeling as pathological features of allergic asthma provoked by house dust mite in vivo.
255 insufficiently controlled moderate-to-severe allergic asthma receiving standard inhaled glucocorticos
256 ons between IgE levels and allergic disease (allergic asthma, rhinitis, and eczema) and between alcoh
258 uring pregnancy is associated with increased allergic asthma risk in the offspring, and given that ap
259 overed DMRs annotated to genes implicated in allergic asthma, Th2 activation and eosinophilia (EPX, I
263 ify Sema3E as a novel regulatory molecule in allergic asthma that acts upstream of proallergic events
264 ies of omalizumab in the treatment of severe allergic asthma that included 4117 unique patients from
265 nknown mode of GC action in the treatment of allergic asthma that might help to develop more specific
266 -severe rhino-conjunctivitis with or without allergic asthma, the cost-effectiveness of SLIT (tablets
268 r IL-13 antagonist as therapeutic agents for allergic asthma through expanding LV mediated-enhanced a
269 airway epithelium and used murine models of allergic asthma to evaluate the relevance of epithelium-
270 were simultaneously associated with asthma, allergic asthma, total IgE, environmental IgE, and FeNO
272 (hi) neutrophils were also needed to mediate allergic asthma triggered by infection with influenza vi
276 data represent a novel approach to treating allergic asthma via regulation of immune response to hou
277 of acute and chronic ovalbumin (OVA)-induced allergic asthma was assessed weekly in CD4(+) T cell-spe
281 mportantly, using a humanized mouse model of allergic asthma, we demonstrate that adoptive transfer o
285 y ceramide and are important for severity of allergic asthma were correlated with ceramide levels mea
287 ry nasal epithelial cells from patients with allergic asthma were found to express increased DUOX1 an
290 and reduced inflammation in a mouse model of allergic asthma, which has a strong neurogenic component
291 . pylori persistence, and protection against allergic asthma, which is a hallmark of H. pylori-infect
292 ore severe IgE-mediated disorders, including allergic asthma, which is driven by the priming of Th2 e
293 l-world setting indicates that patients with allergic asthma who receive AIT are less likely to exper
294 n at the age of 2, prior to the diagnosis of allergic asthma, who are subsequently diagnosed with ast
295 xins on Th2 and Th17 cell development during allergic asthma with a particular emphasis on their role
296 Omalizumab is licensed for therapy in severe allergic asthma with an effect demonstrated after 8 week
298 changes that occur during the development of allergic asthma without genetic and environmental confou
299 emory CD4+ T helper type 2 (Th2) cells drive allergic asthma, yet the mechanisms whereby tissue-resid
300 and air pollution are major risk factors for allergic asthma, yet the mechanistic links between such