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1 ovalbumin-induced severe, steroid-resistant allergic airway disease.
2 of BPEx had no effect on the development of allergic airway disease.
3 enesis and inflammation in a murine model of allergic airway disease.
4 vation of macrophages and is correlated with allergic airway disease.
5 lungs of asthmatic patients and in mice with allergic airway disease.
6 ereas mice treated with R848 did not develop allergic airway disease.
7 acute ovalbumin- and house dust mite-induced allergic airway disease.
8 Ab response and modifies the development of allergic airway disease.
9 xpression associated with the development of allergic airway disease.
10 fine the role of AAMs in the pathogenesis of allergic airway disease.
11 house dust mite (HDM) mouse model of asthma/allergic airway disease.
12 ed in ovalbumin- and house dust mite-induced allergic airway disease.
13 required for the suppression of established allergic airway disease.
14 sential for preventing airway obstruction in allergic airway disease.
15 tic cell cultures and in an in vivo model of allergic airway disease.
16 hlight the importance of the mTOR pathway in allergic airway disease.
17 eactivity (AHR), and ovalbumin (OVA)-induced allergic airway disease.
18 increased apoptosis in 2 distinct models of allergic airway disease.
19 seful tool to combat the rising incidence of allergic airway disease.
20 scription may enhance the risk of developing allergic airway disease.
21 ation in two separate models of Th2-mediated allergic airway disease.
22 s the inflammatory responses associated with allergic airway disease.
23 cule ICOS regulates Th2 effector function in allergic airway disease.
24 s at sites remote from the lung in models of allergic airway disease.
25 ivation and inflammation in a mouse model of allergic airway disease.
26 utritional modifications in a mouse model of allergic airway disease.
27 re not protected from developing OVA-induced allergic airway disease.
28 -induced inflammation in mice as a model for allergic airway disease.
29 ty and prevent the development of Th2-driven allergic airway disease.
30 sitization and the subsequent development of allergic airway disease.
31 hils via CCR3 have a central role in chronic allergic airway disease.
32 ntioxidants and NOX inhibitors in mitigating allergic airway disease.
33 te neutrophils in the pathogenesis of fungal allergic airway disease.
34 nes have not previously been associated with allergic airway disease.
35 l microbiota in promoting the development of allergic airway disease.
36 e the inflammatory processes associated with allergic airway disease.
37 ines in the establishment and maintenance of allergic airway disease.
38 e chemokine receptors CCR3, CCR4 and CCR8 in allergic airway disease.
39 s critical for Th2-mediated responses during allergic airway disease.
40 nesis of inflammation in this mouse model of allergic airway disease.
41 when administrated to mice with established allergic airway disease.
42 ss the biological role of CCR8 in a model of allergic airway disease.
43 to determine its contribution in a model of allergic airway disease.
44 t of airway inflammation in a mouse model of allergic airway disease.
45 siveness and restored steroid sensitivity to allergic airway disease.
46 elease of mediators involved in inflammatory allergic airway disease.
47 fecting Th2 differentiation in this model of allergic airway disease.
48 production in a murine model of OVA-induced allergic airway disease.
49 k ICOS/B7RP-1 interactions in a Th2 model of allergic airway disease.
50 lay an essential role in neutrophil-dominant allergic airway disease.
51 effector Th cells into naive mice to induce allergic airway disease.
52 sponses that arise from A. fumigatus-induced allergic airway disease.
53 in part to the absence of chronic models of allergic airway disease.
54 mucin-stimulating activity of lung fluids in allergic airway disease.
55 ragweed are important in the development of allergic airway disease.
56 iotic metabolite for potential prevention of allergic airway disease.
57 the onset and chronic phase of experimental allergic airway disease.
58 ced AR and in an HDM-induced murine model of allergic airway disease.
59 exacerbating effects of antifungal drugs on allergic airway disease.
60 tis, and also exacerbated the development of allergic airway disease.
61 th PC receptors in the lung protects against allergic airway disease.
62 nt to that of uricase inhibited NO2-promoted allergic airway disease.
63 a in human subjects and with mouse models of allergic airway disease.
64 signalling in AEC regulated key features of allergic airway disease.
65 ytes, and in mice enhance the development of allergic airway disease.
66 ollen and potentially increase occurrence of allergic airway disease.
67 cytokines IL-4 and IL-13 and is activated in allergic airway disease.
68 isin that potentially contribute to initiate allergic airway disease.
69 val Ts E/S in vitro and in a murine model of allergic airway disease.
70 robust TH2 inflammation and exacerbation of allergic airway disease.
71 espiratory syncytial virus (RSV)-exacerbated allergic airway disease.
72 cal for amplifying viral exacerbation during allergic airway disease.
73 33 in regulating airway immune responses and allergic airway diseases.
74 alternative candidate to adult MSCs to treat allergic airway diseases.
75 ght be a therapeutic target in patients with allergic airway diseases.
76 een perceived as a terminal effector cell in allergic airway diseases.
77 key cytokine involved in type 2 immunity and allergic airway diseases.
78 hus may contribute to the pathophysiology of allergic airway diseases.
79 P is a promising potential approach to treat allergic airway diseases.
80 way inflammation in patients with asthma and allergic airway diseases.
81 promotes the development and aggravation of allergic airway diseases.
82 the developing immune system and initiating allergic airway diseases.
83 g therapeutic approaches in the treatment of allergic airway diseases.
84 rested mice that previously developed murine allergic airway diseases.
85 ring the pathophysiology of asthma and other allergic airway diseases.
86 ian populations are increasingly affected by allergic airway diseases.
87 Th2-dependent responses in murine models of allergic airways disease.
88 DAMTS-12 functions in experimental models of allergic airways disease.
89 n HDM-induced glycolysis and pathogenesis of allergic airways disease.
90 and molecules that suppress IL-17-dependent allergic airways disease.
91 strain matched controls in the OVA model of allergic airways disease.
92 onhuman primates with experimentally induced allergic airways disease.
93 ant for maintenance of immune homeostasis in allergic airways disease.
94 in both human asthma and in murine models of allergic airways disease.
95 he regulation of RSV-induced exacerbation of allergic airways disease.
96 elium of asthmatic patients and in mice with allergic airways disease.
97 Rho kinases (ROCKs) contribute to allergic airways disease.
98 metaplasia in a mast cell-dependent model of allergic airways disease.
99 r HDM-induced glycolysis and pathogenesis of allergic airways disease.
100 of susceptibility to fungal allergen-induced allergic airways disease.
101 irway tolerance compromised in patients with allergic airway diseases?
102 wing weaning, susceptibility and severity of allergic airway disease (a murine model of human asthma)
103 cells is necessary and sufficient to elicit allergic airway disease, a mouse model with many feature
104 a biphasic ovalbumin (OVA)-induced model of allergic airway disease (AAD) and its subsequent resolut
106 (C57BL/6J), ovalbumin (OVA)-induced model of allergic airway disease (AAD) at early (3-day OVA-aeroso
108 followed throughout time the development of allergic airway disease (AAD) in both uninfected mice an
114 aride and pneumolysoid (T+P), which suppress allergic airways disease (AAD) in mouse models of asthma
116 ss (AHR) and inflammation in mouse models of allergic airways disease (AAD), associated with inductio
120 pha(-/lox) mice in chronic ovalbumin-induced allergic airway disease, airway hyperreactivity, T(H)2 r
121 of asthma, but the role of Th17 response in allergic airway disease and aging is not well understood
124 ate and adaptive immune responses in chronic allergic airway disease and identify T2M cells as a new
125 Herein we show that pendrin plays a role in allergic airway disease and in regulation of ASL thickne
126 aternal 25(OH)D concentration on outcomes of allergic airway disease and lung function at 20 to 25 ye
127 n D (25[OH]D) concentrations and outcomes of allergic airway disease and lung function in offspring w
128 Additionally, at age 20 years, outcomes of allergic airway disease and lung function were assessed
129 -NO2 is efficacious in preclinical models of allergic airway disease and may have potential for treat
130 exacerbated lung inflammation in a model of allergic airway disease and promoted higher Th2 response
131 were chronically exposed to HDM to establish allergic airway disease and then treated with the EGFR i
132 ils infiltrate airway walls in patients with allergic airway diseases and in animal models of these i
133 pollution (TRAP) exposure is associated with allergic airway diseases and reduced lung function in ch
134 mined in peripheral blood from subjects with allergic airways disease and controls as well as with in
135 ave been linked mechanistically in models of allergic airways disease and have been associated with a
136 a exacerbations, we combined mouse models of allergic airways disease and human rhinovirus infection.
137 s (ODNs), which mimic bacterial DNA, inhibit allergic airways disease and promote responses in the sp
138 e were found to be protected from developing allergic airways disease and showed a marked decrease in
139 ons, and is implicated in obesity, diabetes, allergic airway disease, and altered immune function.
140 e suggest that the severity and character of allergic airway disease are age dependent, with a bias t
141 s by which respiratory infections facilitate allergic airway disease are incompletely understood.
144 acid (OA-NO2) reduced the severity of murine allergic airway disease, as assessed by various patholog
145 ded significant relief from establishment of allergic airways disease, as evident from attenuated Th2
146 wever, both groups of mice exhibited similar allergic airway disease at day 12 after the conidia chal
147 ypically protects against the development of allergic airway disease but may be overcome to induce al
148 thought to contribute to the pathogenesis of allergic airway disease by virtue of their decreased NO
149 However, whether COX inhibition can promote allergic airway diseases by inhibiting immune tolerance
150 viral epitopes in virus inoculated mice with allergic airway disease compared to mice treated with vi
151 ression of CRTh2 was higher in subjects with allergic airways disease compared to controls (P < 0.05)
153 Dermatophagoides farinae-dependent model of allergic airway disease, dextran sodium sulfate-induced
154 sed IL-4Ralpha, those induced in vivo during allergic airway disease did not, possibly rendering them
157 IL-10 signaling in virus-infected mice with allergic airway disease enhanced pulmonary CD4(+) T cell
158 volvement of innate lymphoid cells (ILCs) in allergic airway disease exacerbation caused by high-fat
162 nvironmental factors and immune responses in allergic airway diseases, identification of new allergen
163 ttenuated inflammatory responses redeveloped allergic airway disease if the OVA aerosols were interru
166 sufficient for the development of long-term allergic airway disease in mice and implies that deregul
167 associated with significant exacerbation of allergic airway disease in mice, including an increase i
172 etary intake of methyl donors on the risk of allergic airway disease in offspring in mice and show th
173 through their mother's milk with RSV induced allergic airway disease in response to OVA sensitization
174 and risk factors for the high prevalence of allergic airway disease in the tropical urban environmen
176 with allergens in starting and exacerbating allergic airway diseases in part by production of reacti
178 ) to reverse the increased susceptibility to allergic airways disease in neonatal mice in a model of
179 tivated exhibited characteristic features of allergic airway disease, including airway eosinophilia a
180 tudies in human subjects and mouse models of allergic airway disease indicate a central role of IL-33
181 etect a role for NLRP3 in the development of allergic airway disease induced by either acute or chron
187 ntaining (NLR) family, to the development of allergic airway disease is currently controversial.
190 hyperresponsiveness in RV-infected mice with allergic airways disease is directed in part by eotaxin-
193 results suggest that the presence of AAMs in allergic airway disease may be only an association, as a
194 ed the function of CD137 engagement using an allergic airway disease model in which the mice were sen
198 sion is well established, yet the effects of allergic airway disease on the host response to intra-pu
200 have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged m
201 sitized with cockroach allergen (CRAg), then allergic airway disease parameters were assessed after C
202 enhanced a variety of parameters relevant to allergic airways disease, possibly by altering NO homeos
206 albumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were dev
207 case inhibited the development of OVA-driven allergic airway disease subsequent to OVA challenge, as
212 vo blockade of TIGIT suppressed hallmarks of allergic airway disease, such as lung eosinophilia, gobl
213 e type 2 cytokine IL-13 is a key mediator of allergic airway diseases, such as asthma, and is up-regu
214 nd ILC2 levels are elevated in patients with allergic airway diseases suggest that IL-33 plays an imp
216 with methyl donors enhanced the severity of allergic airway disease that was inherited transgenerati
217 rapeutic effects in mice with fungal-induced allergic airway disease, the highest dose of IL-13-PE te
218 thought to play pivotal roles in asthma and allergic airway diseases, the immunological mechanisms t
219 s positively associated with the etiology of allergic airways disease, the current findings suggest t
220 ary factors can modify the heritable risk of allergic airway disease through epigenetic mechanisms du
221 can interact with allergens in exacerbating allergic airway diseases through generation of reactive
223 urine model of virus-induced exacerbation of allergic airway disease to examine the role of CCR1 on T
224 mite allergen mucosal sensitization model of allergic airway disease to investigate the role of alveo
225 l transfer of protection from development of allergic airway disease to offspring in this model of ma
226 and the role of ORMDL3 in the generation of allergic airways disease to the fungal aeroallergen Alte
227 ed using B7-DC cross-linking Abs, preventing allergic airway disease upon re-exposure to allergen.
229 can exacerbate or trigger the development of allergic airway diseases via multiple mechanisms dependi
234 ith allergen exposure, or the development of allergic airway disease was evaluated in TLR4 or TRIF kn
236 with A. fumigatus conidia, and the resulting allergic airway disease was monitored for up to 37 days.
241 (Runx3), a gene known to negatively regulate allergic airway disease, was found to be excessively met
242 hydrogen peroxide in the pathophysiology of allergic airway disease, we comparatively evaluated mice
243 Using a murine model of neutrophil-dominant allergic airway disease, we demonstrate that BET inhibit
244 ive cell transfer studies in mouse models of allergic airway disease, we examined the effects of Act-
247 sing a robust murine model of antigen-driven allergic airways disease, we have demonstrated that IVIG
249 , rhesus monkeys with experimentally induced allergic airways disease were treated seven times with i
250 ensitization can be the predominant cause of allergic airway diseases, whereas in other environments,
251 HDM translates into increased prevalence of allergic airway diseases, which now impact a large propo
252 a mouse model of RSV-induced exacerbation of allergic airways disease, which mimics hallmark clinical
253 uts together our current knowledge on IgE in allergic airway diseases with a special focus on the ide
254 ILC2s to drive the exacerbation of a murine allergic airway diseases with an eosinophilic phenotype.
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