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1 egulatory role of PTX3 in the development of allergic inflammation.
2 naling and polarization of M2 macrophages in allergic inflammation.
3 vated eosinophils in tissue is a hallmark of allergic inflammation.
4 xploited to control both innate and adaptive allergic inflammation.
5 firming its essential role in inhibiting the allergic inflammation.
6 hind the stimulatory effects of IL-10 during allergic inflammation.
7 ic pathways to favor persistence at sites of allergic inflammation.
8 rgely been characterized in murine models of allergic inflammation.
9 rgy (sensitization and total serum IgE), and allergic inflammation.
10 l and basophil activation and thus immediate allergic inflammation.
11 obesity and IL-4 can synergize to exacerbate allergic inflammation.
12 e H4R during ontogeny and development of the allergic inflammation.
13 eosinophil recruitment as it unfolds during allergic inflammation.
14 lar packaging and extracellular functions in allergic inflammation.
15 -33/ST2 signaling that triggers Th2-dominant allergic inflammation.
16 a therapeutic target for particulate-induced allergic inflammation.
17 ng may augment STAT6-independent pathways of allergic inflammation.
18 s have a central role in orchestrating local allergic inflammation.
19 roup 2 innate lymphoid cells (ILC2s) promote allergic inflammation.
20 plore a novel pollen/TLR4 innate immunity in allergic inflammation.
21 ism by which IgE-allergen complexes regulate allergic inflammation.
22 ress cytokines yet not sufficient to control allergic inflammation.
23 seases in which ILCs are implicated, such as allergic inflammation.
24 e activity and initiating the development of allergic inflammation.
25 an inflammatory signaling loop that promotes allergic inflammation.
26 lls subjected to acute and chronic models of allergic inflammation.
27 sing normal AMs to cytokines associated with allergic inflammation.
28 nt allergen sensitization and subsequent Th2 allergic inflammation.
29 ogenous maresin 1 (MaR1) during self-limited allergic inflammation.
30 e tolerogenic responses to allergens incites allergic inflammation.
31 -13, a cytokine required for many aspects of allergic inflammation.
32 Basophils play a pivotal role in allergic inflammation.
33 erve as innate host defense molecules during allergic inflammation.
34 landin D2 (PGD2 ) plays an important role in allergic inflammation.
35 in regulating eotaxin-3 production in human allergic inflammation.
36 lates a range of immune responses, including allergic inflammation.
37 hoid cell (ILC2) activation to induce innate allergic inflammation.
38 rs spontaneous AHR in mice in the absence of allergic inflammation.
39 ses and more importantly did not develop any allergic inflammation.
40 f misoprostol during sensitization inhibited allergic inflammation.
41 to the pathology of autoimmune diseases and allergic inflammation.
42 e at tissue barriers that are susceptible to allergic inflammation.
43 that the Rab27 effector, exophilin-5, has in allergic inflammation.
44 s predominantly stimulate Th2 cells, causing allergic inflammation.
45 as capable of initiating severe, rapid onset allergic inflammation.
46 es to influence systemic responses including allergic inflammation.
47 nature of these receptors, and the effect on allergic inflammation.
48 cytokine that may be important in initiating allergic inflammation.
49 gulatory B cells participates to more severe allergic inflammation.
50 esponse that facilitates eosinophil-mediated allergic inflammation.
51 NA sensing by T cells to trigger and amplify allergic inflammation.
52 , by contrast, resulted in an attenuation of allergic inflammation.
53 lls has been implicated as a key mediator of allergic inflammation.
54 population of macrophages is associated with allergic inflammation.
55 for ORMDL3 in eosinophils in the context of allergic inflammation.
56 posure on the regulation of DC functions and allergic inflammation.
57 dentifying CD63 as an important component of allergic inflammation.
58 notype and contributes to the development of allergic inflammation.
59 be an important feature of sustained chronic allergic inflammation.
60 therapeutic target for the downregulation of allergic inflammation.
61 nd suggest a new effect on their function in allergic inflammation.
62 ealed the strong linkage between obesity and allergic inflammation.
63 , activation, and function in the context of allergic inflammation.
64 mote lung mast cell infiltration and augment allergic inflammation.
65 leviating the development and progression of allergic inflammation.
66 o analyze whether ATIs are also modifiers of allergic inflammation.
67 hemokine production, thereby contributing to allergic inflammation.
68 cosal epithelial/subepithelial DC network in allergic inflammation.
69 o the release of type 2 cytokines that drive allergic inflammation.
70 IgE is both a marker and mediator of allergic inflammation.
71 terminants for the magnitude of IgE-mediated allergic inflammation.
72 , with a specific focus on the mechanisms of allergic inflammation.
73 efine a requirement for IL-9 in TSLP-induced allergic inflammation.
74 h focus on molecular and cellular aspects of allergic inflammation.
75 st defense against helminth parasites and in allergic inflammation.
76 IL-13 is a critical effector cytokine for allergic inflammation.
77 development of T helper (Th2) cell-mediated allergic inflammation.
78 in several inflammatory processes including allergic inflammation.
79 odels suggest exposure to BPA might increase allergic inflammation.
80 rticularly in the late and chronic stages of allergic inflammation.
81 4 consecutive days to evaluate innate airway allergic inflammation.
82 omalizumab completely abolished ATI-induced allergic inflammation.
83 mphoid cells (ILC2s) that may act throughout allergic inflammation.
84 were initially thought to act only early in allergic inflammation.
85 in both a steady-state situation and during allergic inflammation.
86 ence for a protective role of these cells in allergic inflammation.
87 hil accumulation in the setting of pulmonary allergic inflammation.
88 s the role of Blimp-1 in the pathogenesis of allergic inflammation.
89 tibodies do not protect against IgE-mediated allergic inflammation.
90 ulator of T(H)9 differentiation and controls allergic inflammation.
91 compounds in reducing Alternaria-stimulated allergic inflammation.
92 dysregulation manifesting as autoimmunity or allergic inflammation.
93 ient subpopulation with increased esophageal allergic inflammation.
94 described to regulate adaptive responses in allergic inflammation.
95 cells of the innate immune system linked to allergic inflammation.
96 l as important future research directions in allergic inflammation.
97 ected by the absence of Sema4C expression in allergic inflammation.
98 tration of NMU with IL-25 strongly amplified allergic inflammation.
99 ctive roles in the lung, particularly during allergic inflammation.
100 , influencing the immunological character of allergic inflammation.
101 lls (ILC2s) are tissue sentinel mediators of allergic inflammation.
103 e the role of IL-22 in antigen-driven airway allergic inflammation after inhalation challenge in epic
104 eficiency abrogated the protective effect of allergic inflammation against S. pneumoniae pathogenesis
105 that functional inhibition of PAR2 prevents allergic inflammation, AHR and airway remodeling in chro
106 pithelium and may coordinately contribute to allergic inflammation, AHR, and fibrotic airway remodeli
108 nt roles in mast cell-dependent, OVA-induced allergic inflammation and AHR, in part by regulating the
109 n of T-cell-derived vs innate IL-4/IL-13 for allergic inflammation and airway hyperreactivity remains
110 he airways is involved in the development of allergic inflammation and airway hyperresponsiveness (AH
112 the mechanisms underlying the initiation of allergic inflammation and allergen induced anaphylaxis a
113 ied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of cell-base
114 ied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of Th9 diffe
115 phosphatase SHP-1 plays an important role in allergic inflammation and anaphylaxis and determined whe
120 effective producers of IL-5 and IL-13 during allergic inflammation and bridge the innate and adaptive
121 studies evaluating the relationship between allergic inflammation and cancer have revealed conflicti
122 Enhancement of the regulatory response to allergic inflammation and changes in the Th2/Th1 balance
123 e differentially regulated in the context of allergic inflammation and discuss the therapeutic potent
125 HIF-1alpha in vivo, significantly decreased allergic inflammation and eosinophilia induced by allerg
126 model, we evaluated the relationship between allergic inflammation and features of remodelling in AR.
127 urine model was used to study the effects of allergic inflammation and FP treatment on transmucosal p
128 ases of the gastrointestinal tract caused by allergic inflammation and gastrointestinal dysfunction.
132 s a critical role as a negative regulator in allergic inflammation and in allergen induced anaphylaxi
133 nduced EMH contributes to the development of allergic inflammation and indicate that EMH is a conserv
136 e IgE- and T-cell-mediated manifestations of allergic inflammation and may be important for the devel
137 harmacological approach for the treatment of allergic inflammation and other eosinophil-driven disord
138 harmacological approach for the treatment of allergic inflammation and other eosinophilic disorders.
139 ells are a major source of IL-9 in models of allergic inflammation and play an important role in mast
140 trating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inf
141 hem, IL-25 has been shown to be important in allergic inflammation and protection against parasitic i
143 ked NKG2D were resistant to the induction of allergic inflammation and showed little pulmonary eosino
144 tance of plasma cells as regulatory cells in allergic inflammation and suggests that CD138(+) B cells
145 nflammatory responses at mucosal barriers in allergic inflammation and targeting TSLP-mediated signal
146 ophageal-specific genetic risk variants; and allergic inflammation and that the disease is remitted b
148 methodologies: the secretion of mediators of allergic inflammation and the expression of proteins on
149 y has been identified as a crucial driver of allergic inflammation and tight junction dysfunction.
150 hypotheses are based on known mechanisms of allergic inflammation and/or IgE antibody functions, and
151 critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (
152 h the allergen, could synergistically elicit allergic inflammation, and aryl hydrocarbon receptor (Ah
154 sents with various manifestations, including allergic inflammation, and has emerged as an alarming pu
156 PSA, negatively regulated HDAC3 expression, allergic inflammation, and the positive feedback regulat
157 tions have emerged as critical modulators of allergic inflammation, and type 2 innate lymphoid cells
160 uggest that dsRNA challenges superimposed on allergic inflammation are suited for pharmacological stu
162 on gestational day 15, which produced robust allergic inflammation, as measured by elevated immunoglo
165 emerged as key players in the development of allergic inflammation at multiple barrier surfaces.
166 which the immune system induces and controls allergic inflammation at the T-cell epitope level is cri
167 que opportunity to probe the pathogenesis of allergic inflammation at the tissue level through readil
168 Because of the link between T(H)9 cells and allergic inflammation, autoimmunity, and antitumor surve
169 mphopoietin (TSLP), a cytokine that promotes allergic inflammation, but how TSLP might contribute to
171 LP promoted IL-9-dependent, Th9 cell-induced allergic inflammation by acting directly on T cells.
172 Cysteine proteases are potent triggers of allergic inflammation by causing barrier disruption in l
173 pplied THC can effectively attenuate contact allergic inflammation by decreasing keratinocyte-derived
174 forming growth factor-beta, and induction of allergic inflammation by eosinophils and mast cells.
175 little remains known about the regulation of allergic inflammation by glutathione S-transferase P1 in
176 pG oligodeoxynucleotides downmodulate airway allergic inflammation by mechanisms dependent on T-cell
177 P) has been implicated in the development of allergic inflammation by promoting Th2-type responses an
178 es the airways for antigen challenge-induced allergic inflammation characterized by the presence of b
179 ndent monocyte-derived DCs exhibited similar allergic inflammation compared with their wild-type coun
180 ression had a diminished capacity to promote allergic inflammation compared with wild-type controls.
181 CR4 deficiency displayed an augmented airway allergic inflammation compared with wild-type or CCR2 kn
182 vated basophils, which are effector cells in allergic inflammation, contribute to the progress of col
183 ther studies are needed to determine whether allergic inflammation contributes toward epileptogenesis
185 o bacterial skin infections, suggesting that allergic inflammation curtails neutrophil responses.
187 RATIONALE: Leukocyte recruitment to sites of allergic inflammation depends on the local production of
188 ce of adjuvant, in which mast cell-dependent allergic inflammation develops, significantly reduced OV
190 g1(-/-) mice subjected to a chronic model of allergic inflammation displayed reduced mast cell infilt
191 cells yet were resistant to the induction of allergic inflammation exemplified by diminished airway e
192 ogeneity of human tissue CD3+ T cells during allergic inflammation, focusing on a tissue-specific all
193 del of house dust mite-induced (HDM-induced) allergic inflammation followed by Ascaris infection to d
194 they were metabolically reprogrammed to skew allergic inflammation from eosinophilic T helper cell 2
197 , the role of apolipoprotein-IV (ApoA-IV) in allergic inflammation has not been addressed thoroughly
198 in pollen- and cat dander-induced innate and allergic inflammation has not been critically evaluated.
199 to play important roles in the initiation of allergic inflammation; however, it is unclear whether li
205 t the hypothesis that NTN could modulate the allergic inflammation in different mouse asthma models.
206 a shed light on the principles that underlie allergic inflammation in different tissues and highlight
211 cialized for the production of IL-9, promote allergic inflammation in mice, and are associated with a
216 may reflect distinct phenotypic features of allergic inflammation in older patients with asthma.
217 +) iNKT cell population leads to exacerbated allergic inflammation in the airways upon intranasal imm
220 , we aimed to assess the association between allergic inflammation in the lung (asthma), skin (eczema
222 tigen treatment was also capable of inducing allergic inflammation in the lung, resulting in anti-Pne
223 V5 in T cells results in distinct effects on allergic inflammation in the lung, suggesting that these
225 ults suggest that urban PM2.5 may exacerbate allergic inflammation in the murine lung via a TLR2/TLR4
226 gate a role for miR-155 in the regulation of allergic inflammation in vivo, we used miR-155 knockout
227 pression was required for IgE-driven chronic allergic inflammation in vivo, whereas STIM2 was require
229 iency had little effect on the parameters of allergic inflammation, including cell counts in bronchoa
230 otent activator of various cells involved in allergic inflammation, including eosinophils and mast ce
231 s in regulating key pathogenic mechanisms in allergic inflammation, including polarization of adaptiv
233 weight gain in an experimental model of lung allergic inflammation induced by chicken egg ovalbumin (
234 ight to clarify the underlying mechanisms of allergic inflammation-induced psychiatric disorders rela
239 ent of purine activation of platelets during allergic inflammation is distinct from purine involvemen
241 or allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment
244 nce that in both OVA and HDM mouse models of allergic inflammation, LAPCs accumulate in the lungs and
245 sistance to helminth infection, promotion of allergic inflammation, metabolic homeostasis and tissue
247 nexin V positivity, P < .005), and less lung allergic inflammation (number of lung eosinophils, P < .
249 egrin receptors on ASM opposes the effect of allergic inflammation on RhoA activity and identify a pa
250 sessed the impact of ovalbumin (OVA)-induced allergic inflammation on the appearance of anxiety-like
251 rect experimental evidence for the effect of allergic inflammation on the structure and function of m
252 ction of mast cells in patients with chronic allergic inflammation or the effect of repeated Fcepsilo
253 mportant in effector functions for eliciting allergic inflammation, parasite defense, epithelial repa
254 ing acute inflammation, autoimmune diseases, allergic inflammation, pregnancy, cancer, and infection.
255 We investigated HDAC3 involvement in the allergic inflammation-promotion of metastatic potential
256 rly that associated with classic features of allergic inflammation, provides new insight into potenti
257 rgy pathway (linking allergen sensitization, allergic inflammation, pulmonary physiology, and rhiniti
258 risk-factor domains (allergen sensitization, allergic inflammation, pulmonary physiology, stress, obe
266 memory CD4(+) T helper 2 (TH2) cells during allergic inflammation requires their recruitment into th
267 mediators, as well as late-phase and chronic allergic inflammation, resulting from T-cell, basophil,
268 ient ILC2s had reduced capability to promote allergic inflammation, resulting in increased resistance
269 2 cells and eosinophils are hallmarks of the allergic inflammation seen in patients with allergic rhi
270 To examine Treg and STAT6 interaction during allergic inflammation, STAT6(-/-), STAT6xRAG2(-/-), and
271 and work performance during periods of acute allergic inflammation, supporting the idea of an impact
272 atory environments, our data suggest that in allergic inflammation, Th17 cells are comparatively stab
274 essing BATF were more efficient at promoting allergic inflammation than control transduced cells.
275 we show that Muc5ac is a central effector of allergic inflammation that is required for airway hyperr
276 oduction, peri-vascular, peri-bronchial, and allergic inflammation that was unresponsive to inhaled c
278 sion and function of miRNAs in patients with allergic inflammation, their role as disease biomarkers,
279 for IgE, FcepsilonRII (CD23), contributes to allergic inflammation through allergen presentation to T
280 nct biological functions: free IgE initiated allergic inflammation through FcepsilonRI on allergic ef
281 odels suggests that these cells downregulate allergic inflammation through IFN-gamma production.
282 licated in the initiation and progression of allergic inflammation through its ability to activate de
283 at platelets may also contribute directly to allergic inflammation, through alterations in lung funct
285 used a mouse model for IgE-dependent chronic allergic inflammation to study the role of basophils and
286 a higher saEPI along with higher markers of allergic inflammation, treatment step, and a recent exac
288 lonRI on mast cells and basophils and drives allergic inflammation upon secondary allergen contact.
290 associated pulmonary inflammation, and human allergic inflammation was associated with reduced expres
293 Interestingly, although the DEP-enhanced allergic inflammation was marginally reduced in ILC2-def
294 ays inflammation in ROCK2-insufficient mice, allergic inflammation was not different in ROCK2(CD)(4Cr
295 l asthma wherein infection during heightened allergic inflammation was protective against influenza A
299 absence of TSLPR have a drastic reduction of allergic inflammation with diminished eosinophil recruit
300 nscriptomes of single cells in patients with allergic inflammation with high resolution in the contex