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1 e activity and initiating the development of allergic inflammation.
2 an inflammatory signaling loop that promotes allergic inflammation.
3 lls subjected to acute and chronic models of allergic inflammation.
4 ogenous maresin 1 (MaR1) during self-limited allergic inflammation.
5 e tolerogenic responses to allergens incites allergic inflammation.
6 -13, a cytokine required for many aspects of allergic inflammation.
7 erve as innate host defense molecules during allergic inflammation.
8 landin D2 (PGD2 ) plays an important role in allergic inflammation.
9 in regulating eotaxin-3 production in human allergic inflammation.
10 lates a range of immune responses, including allergic inflammation.
11 rs spontaneous AHR in mice in the absence of allergic inflammation.
12 ses and more importantly did not develop any allergic inflammation.
13 f misoprostol during sensitization inhibited allergic inflammation.
14 to the pathology of autoimmune diseases and allergic inflammation.
15 e at tissue barriers that are susceptible to allergic inflammation.
16 s predominantly stimulate Th2 cells, causing allergic inflammation.
17 as capable of initiating severe, rapid onset allergic inflammation.
18 es to influence systemic responses including allergic inflammation.
19 nature of these receptors, and the effect on allergic inflammation.
20 cytokine that may be important in initiating allergic inflammation.
21 gulatory B cells participates to more severe allergic inflammation.
22 esponse that facilitates eosinophil-mediated allergic inflammation.
23 NA sensing by T cells to trigger and amplify allergic inflammation.
24 , by contrast, resulted in an attenuation of allergic inflammation.
25 lls has been implicated as a key mediator of allergic inflammation.
26 population of macrophages is associated with allergic inflammation.
27 for ORMDL3 in eosinophils in the context of allergic inflammation.
28 posure on the regulation of DC functions and allergic inflammation.
29 dentifying CD63 as an important component of allergic inflammation.
30 notype and contributes to the development of allergic inflammation.
31 be an important feature of sustained chronic allergic inflammation.
32 therapeutic target for the downregulation of allergic inflammation.
33 nd suggest a new effect on their function in allergic inflammation.
34 , activation, and function in the context of allergic inflammation.
35 mote lung mast cell infiltration and augment allergic inflammation.
36 ected by the absence of Sema4C expression in allergic inflammation.
37 leviating the development and progression of allergic inflammation.
38 hemokine production, thereby contributing to allergic inflammation.
39 cosal epithelial/subepithelial DC network in allergic inflammation.
40 tration of NMU with IL-25 strongly amplified allergic inflammation.
41 IgE is both a marker and mediator of allergic inflammation.
42 terminants for the magnitude of IgE-mediated allergic inflammation.
43 , with a specific focus on the mechanisms of allergic inflammation.
44 efine a requirement for IL-9 in TSLP-induced allergic inflammation.
45 h focus on molecular and cellular aspects of allergic inflammation.
46 st defense against helminth parasites and in allergic inflammation.
47 IL-13 is a critical effector cytokine for allergic inflammation.
48 development of T helper (Th2) cell-mediated allergic inflammation.
49 in several inflammatory processes including allergic inflammation.
50 odels suggest exposure to BPA might increase allergic inflammation.
51 rticularly in the late and chronic stages of allergic inflammation.
52 est that memIL-13Ralpha2 might contribute to allergic inflammation.
53 xygenase (IDO), is a critical participant in allergic inflammation.
54 ctive roles in the lung, particularly during allergic inflammation.
55 ice to study cytokine-producing cells during allergic inflammation.
56 ature of lesional AD pathology comorbid with allergic inflammation.
57 egatively influences Th2 differentiation and allergic inflammation.
58 detected at high concentrations at sites of allergic inflammation.
59 d basophil-mediated T(H)2 cell responses and allergic inflammation.
60 that establish the IDO pathway as central to allergic inflammation.
61 othelial SK-1 is an important contributor to allergic inflammation.
62 apeutic options for the management of ocular allergic inflammation.
63 tion in mast cells, which is a mechanism for allergic inflammation.
64 ses to pathogens and subsequently exacerbate allergic inflammation.
65 , influencing the immunological character of allergic inflammation.
66 romotes pathologic responses associated with allergic inflammation.
67 sed by Th2 cells and other cells involved in allergic inflammation.
68 rapeutics as predicted from animal models of allergic inflammation.
69 may have important clinical implications in allergic inflammation.
70 airway diseases that are linked to atopy and allergic inflammation.
71 ven eotaxin-3 in the pathogenesis of chronic allergic inflammation.
72 decreased resolvin E1-mediated resolution of allergic inflammation.
73 ne 3 in the inflamed tissue of patients with allergic inflammation.
74 hance the therapeutic efficacy of CpG during allergic inflammation.
75 gulating the balance of airway tolerance and allergic inflammation.
76 dysregulation manifesting as autoimmunity or allergic inflammation.
77 lls (ILC2s) are tissue sentinel mediators of allergic inflammation.
78 egulatory role of PTX3 in the development of allergic inflammation.
79 naling and polarization of M2 macrophages in allergic inflammation.
80 vated eosinophils in tissue is a hallmark of allergic inflammation.
81 ient subpopulation with increased esophageal allergic inflammation.
82 xploited to control both innate and adaptive allergic inflammation.
83 firming its essential role in inhibiting the allergic inflammation.
84 hind the stimulatory effects of IL-10 during allergic inflammation.
85 ic pathways to favor persistence at sites of allergic inflammation.
86 rgely been characterized in murine models of allergic inflammation.
87 rgy (sensitization and total serum IgE), and allergic inflammation.
88 l and basophil activation and thus immediate allergic inflammation.
89 obesity and IL-4 can synergize to exacerbate allergic inflammation.
90 described to regulate adaptive responses in allergic inflammation.
91 e H4R during ontogeny and development of the allergic inflammation.
92 eosinophil recruitment as it unfolds during allergic inflammation.
93 -33/ST2 signaling that triggers Th2-dominant allergic inflammation.
94 a therapeutic target for particulate-induced allergic inflammation.
95 ng may augment STAT6-independent pathways of allergic inflammation.
96 s have a central role in orchestrating local allergic inflammation.
97 roup 2 innate lymphoid cells (ILC2s) promote allergic inflammation.
98 plore a novel pollen/TLR4 innate immunity in allergic inflammation.
99 ism by which IgE-allergen complexes regulate allergic inflammation.
100 cells of the innate immune system linked to allergic inflammation.
101 ress cytokines yet not sufficient to control allergic inflammation.
102 seases in which ILCs are implicated, such as allergic inflammation.
104 that functional inhibition of PAR2 prevents allergic inflammation, AHR and airway remodeling in chro
105 pithelium and may coordinately contribute to allergic inflammation, AHR, and fibrotic airway remodeli
107 nt roles in mast cell-dependent, OVA-induced allergic inflammation and AHR, in part by regulating the
108 n of T-cell-derived vs innate IL-4/IL-13 for allergic inflammation and airway hyperreactivity remains
109 he airways is involved in the development of allergic inflammation and airway hyperresponsiveness (AH
110 -source d-alpha-tocopheryl acetate modulates allergic inflammation and airway hyperresponsiveness in
112 the mechanisms underlying the initiation of allergic inflammation and allergen induced anaphylaxis a
113 reactivity and had reduced ability to induce allergic inflammation and allergic responses but induced
114 ied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of cell-base
115 ied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of Th9 diffe
116 phosphatase SHP-1 plays an important role in allergic inflammation and anaphylaxis and determined whe
118 ytokine responses promote the development of allergic inflammation and are critical for immunity to p
119 to play a central role in manifestations of allergic inflammation and are found in the epithelium in
123 Enhancement of the regulatory response to allergic inflammation and changes in the Th2/Th1 balance
124 e differentially regulated in the context of allergic inflammation and discuss the therapeutic potent
125 e set correlates with physiologic markers of allergic inflammation and disease in rhesus asthma.
127 HIF-1alpha in vivo, significantly decreased allergic inflammation and eosinophilia induced by allerg
128 te a previously unidentified role for H2R in allergic inflammation and establishes a synergy between
129 urine model was used to study the effects of allergic inflammation and FP treatment on transmucosal p
134 s a critical role as a negative regulator in allergic inflammation and in allergen induced anaphylaxi
135 nduced EMH contributes to the development of allergic inflammation and indicate that EMH is a conserv
138 e IgE- and T-cell-mediated manifestations of allergic inflammation and may be important for the devel
139 harmacological approach for the treatment of allergic inflammation and other eosinophilic disorders.
140 ells are a major source of IL-9 in models of allergic inflammation and play an important role in mast
141 trating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inf
142 hem, IL-25 has been shown to be important in allergic inflammation and protection against parasitic i
144 inophils are the major cellular effectors of allergic inflammation and represent an important therape
145 lymphocytes are pathogenically important in allergic inflammation and sensitive to Fas-mediated apop
147 ked NKG2D were resistant to the induction of allergic inflammation and showed little pulmonary eosino
148 tance of plasma cells as regulatory cells in allergic inflammation and suggests that CD138(+) B cells
149 ophageal-specific genetic risk variants; and allergic inflammation and that the disease is remitted b
151 methodologies: the secretion of mediators of allergic inflammation and the expression of proteins on
152 hypotheses are based on known mechanisms of allergic inflammation and/or IgE antibody functions, and
153 critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (
154 h the allergen, could synergistically elicit allergic inflammation, and aryl hydrocarbon receptor (Ah
156 basophil- and IgE-dependent model of chronic allergic inflammation, and do not develop IgE-dependent
157 sents with various manifestations, including allergic inflammation, and has emerged as an alarming pu
160 PSA, negatively regulated HDAC3 expression, allergic inflammation, and the positive feedback regulat
163 uggest that dsRNA challenges superimposed on allergic inflammation are suited for pharmacological stu
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 were typically confined to the airway during allergic inflammation but became locally invasive and di
168 mphopoietin (TSLP), a cytokine that promotes allergic inflammation, but how TSLP might contribute to
169 -phase allergic reactions (LPRs) and chronic allergic inflammation, but its functions during asthma a
170 T cells in various model systems, including allergic inflammation, but the factors being involved in
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 ndent monocyte-derived DCs exhibited similar allergic inflammation compared with their wild-type coun
179 ression had a diminished capacity to promote allergic inflammation compared with wild-type controls.
180 CR4 deficiency displayed an augmented airway allergic inflammation compared with wild-type or CCR2 kn
181 vated basophils, which are effector cells in allergic inflammation, contribute to the progress of col
182 ther studies are needed to determine whether allergic inflammation contributes toward epileptogenesis
184 o bacterial skin infections, suggesting that allergic inflammation curtails neutrophil responses.
186 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
189 g1(-/-) mice subjected to a chronic model of allergic inflammation displayed reduced mast cell infilt
190 cells yet were resistant to the induction of allergic inflammation exemplified by diminished airway e
191 a expressions to modulate the elicitation of allergic inflammation following ovalbumin (OVA) challeng
192 they were metabolically reprogrammed to skew allergic inflammation from eosinophilic T helper cell 2
196 in pollen- and cat dander-induced innate and allergic inflammation has not been critically evaluated.
198 ith the recognition that asthma is more than allergic inflammation, has drawn attention to the innate
199 ed in induction of T helper 2 (Th2)-mediated allergic inflammation, has recently been shown to stimul
200 to play important roles in the initiation of allergic inflammation; however, it is unclear whether li
203 nd tissue remodeling associated with chronic allergic inflammation in asthma and other settings.
208 t the hypothesis that NTN could modulate the allergic inflammation in different mouse asthma models.
213 cialized for the production of IL-9, promote allergic inflammation in mice, and are associated with a
215 cking by the chemokine system contributes to allergic inflammation in mouse models and in human aller
218 may reflect distinct phenotypic features of allergic inflammation in older patients with asthma.
219 gE recognition of autoantigens might augment allergic inflammation in the absence of exogenous allerg
220 +) iNKT cell population leads to exacerbated allergic inflammation in the airways upon intranasal imm
222 associated with asthma induces eosinophilic allergic inflammation in the lung, and mammalian chitina
223 supplementation can decrease the severity of allergic inflammation in the lung, potentially via multi
224 tigen treatment was also capable of inducing allergic inflammation in the lung, resulting in anti-Pne
225 V5 in T cells results in distinct effects on allergic inflammation in the lung, suggesting that these
227 ron supplementation affected the severity of allergic inflammation in the lungs, using a classic mode
228 ults suggest that urban PM2.5 may exacerbate allergic inflammation in the murine lung via a TLR2/TLR4
229 gate a role for miR-155 in the regulation of allergic inflammation in vivo, we used miR-155 knockout
233 iency had little effect on the parameters of allergic inflammation, including cell counts in bronchoa
234 otent activator of various cells involved in allergic inflammation, including eosinophils and mast ce
235 s in regulating key pathogenic mechanisms in allergic inflammation, including polarization of adaptiv
236 rrelated with systemic and local measures of allergic inflammation, including serum IgE levels, blood
242 ent of purine activation of platelets during allergic inflammation is distinct from purine involvemen
243 or allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment
246 y player in the induction and maintenance of allergic inflammation, it represents a prime target for
247 nce that in both OVA and HDM mouse models of allergic inflammation, LAPCs accumulate in the lungs and
248 sistance to helminth infection, promotion of allergic inflammation, metabolic homeostasis and tissue
251 nexin V positivity, P < .005), and less lung allergic inflammation (number of lung eosinophils, P < .
255 hil-dependent reaction, IgE-mediated chronic allergic inflammation of the skin, but respond normally
256 egrin receptors on ASM opposes the effect of allergic inflammation on RhoA activity and identify a pa
257 ction of mast cells in patients with chronic allergic inflammation or the effect of repeated Fcepsilo
258 mportant in effector functions for eliciting allergic inflammation, parasite defense, epithelial repa
259 ing acute inflammation, autoimmune diseases, allergic inflammation, pregnancy, cancer, and infection.
260 d associations with family history, obesity, allergic inflammation, prior infection, absence of ART,
261 We investigated HDAC3 involvement in the allergic inflammation-promotion of metastatic potential
262 rly that associated with classic features of allergic inflammation, provides new insight into potenti
263 rgy pathway (linking allergen sensitization, allergic inflammation, pulmonary physiology, and rhiniti
264 risk-factor domains (allergen sensitization, allergic inflammation, pulmonary physiology, stress, obe
272 memory CD4(+) T helper 2 (TH2) cells during allergic inflammation requires their recruitment into th
273 mediators, as well as late-phase and chronic allergic inflammation, resulting from T-cell, basophil,
274 ient ILC2s had reduced capability to promote allergic inflammation, resulting in increased resistance
275 2 cells and eosinophils are hallmarks of the allergic inflammation seen in patients with allergic rhi
276 To examine Treg and STAT6 interaction during allergic inflammation, STAT6(-/-), STAT6xRAG2(-/-), and
277 and work performance during periods of acute allergic inflammation, supporting the idea of an impact
278 atory environments, our data suggest that in allergic inflammation, Th17 cells are comparatively stab
280 essing BATF were more efficient at promoting allergic inflammation than control transduced cells.
281 we show that Muc5ac is a central effector of allergic inflammation that is required for airway hyperr
282 oduction, peri-vascular, peri-bronchial, and allergic inflammation that was unresponsive to inhaled c
283 sion and function of miRNAs in patients with allergic inflammation, their role as disease biomarkers,
284 for IgE, FcepsilonRII (CD23), contributes to allergic inflammation through allergen presentation to T
285 licated in the initiation and progression of allergic inflammation through its ability to activate de
286 at platelets may also contribute directly to allergic inflammation, through alterations in lung funct
289 a higher saEPI along with higher markers of allergic inflammation, treatment step, and a recent exac
294 Interestingly, although the DEP-enhanced allergic inflammation was marginally reduced in ILC2-def
295 ays inflammation in ROCK2-insufficient mice, allergic inflammation was not different in ROCK2(CD)(4Cr
296 l asthma wherein infection during heightened allergic inflammation was protective against influenza A
299 STAT6-dependent and -independent features of allergic inflammation, which may impact treatments targe
300 absence of TSLPR have a drastic reduction of allergic inflammation with diminished eosinophil recruit
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