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1 in conjunctival tissue during an OVA-induced allergic response.
2 ucosal tissue that results in the late-phase allergic response.
3 s of mice undergoing house dust mite-induced allergic response.
4 signaling pathways in the initiation of the allergic response.
5 teolytic activity contributes to the overall allergic response.
6 poietin secretion and a cutaneous T-helper 2 allergic response.
7 possibly having a role in IgG modulation of allergic response.
8 (TSLP) secretion and a cutaneous T-helper 2 allergic response.
9 CFP to allergic recipients downmodulated the allergic response.
10 se are downregulated by Th2 cytokines of the allergic response.
11 development of Th2 cells and the subsequent allergic response.
12 nse to TSLP by CD4 T cells in vivo during an allergic response.
13 T mice, which did not exhibit an OVA-induced allergic response.
14 resentation, and (may) thereby influence the allergic response.
15 ature coincident with the suppression of the allergic response.
16 exercise-induced asthma, and the late-phase allergic response.
17 itical role in the development of Brazil nut-allergic response.
18 ing sensitization and challenge phases of an allergic response.
19 mast cells and basophils in the food-induced allergic response.
20 e promising candidates for modulation of the allergic response.
21 ls, and trigger inflammatory cascades of the allergic response.
22 te inflammatory pathways associated with the allergic response.
23 play pivotal roles in the initiation of the allergic response.
24 ell degranulation is a critical component of allergic response.
25 lium and influence the initiation of the HDM-allergic response.
26 ntibodies were the effector molecules of the allergic response.
27 tes mast cells and basophils, initiating the allergic response.
28 importance of B cells in maintenance of the allergic response.
29 r activation of the immune system during the allergic response.
30 ss to adenosine, could be useful to suppress allergic responses.
31 attempted to prenatally abolish or diminish allergic responses.
32 ipients fails to restore development of lung allergic responses.
33 demonstrated to contribute to modulation of allergic responses.
34 p110delta-selective inhibitor idelalisib on allergic responses.
35 relating ozone to respiratory infections and allergic responses.
36 Mast cells play an important role in allergic responses.
37 often leads to T helper 2 (Th2) cell-driven allergic responses.
38 ongylus brasiliensis to induce innate type 2 allergic responses.
39 resident Th2 memory cells as drivers of lung allergic responses.
40 that can both promote and curb Th2-dependent allergic responses.
41 t to function as an adjuvant that can induce allergic responses.
42 ling in Th2 cytokine-driven inflammation and allergic responses.
43 immunomodulatory properties of histamine in allergic responses.
44 ophils, which contribute to the pathology of allergic responses.
45 thought to play a role in the development of allergic responses.
46 Mast cells play critical roles in allergic responses.
47 's critical involvement in the regulation of allergic responses.
48 D25(+) T cells, enhanced development of lung allergic responses.
49 xploited therapeutically for modification of allergic responses.
50 supports its role as a mediator of immediate allergic responses.
51 DC migration and subsequent modification of allergic responses.
52 n CD4(+) T cells showed markedly ameliorated allergic responses.
53 exogenous stimulation and may contribute to allergic responses.
54 tions between them are essential to maximize allergic responses.
55 modulating adaptive immunity during chronic allergic responses.
56 major allergen and is responsible for severe allergic responses.
57 inase (PI3K) isoforms in sequential steps to allergic responses.
58 STAT6 plays a central role in IL-4-mediated allergic responses.
59 nsitization and whether recruitment promotes allergic responses.
60 e molecular interactions taking place during allergic responses.
61 hat has been implicated in the initiation of allergic responses.
62 is a costimulatory molecule involved in Th2 allergic responses.
63 otential proresolving therapeutic agents for allergic responses.
64 ng contributes to the effector phase of some allergic responses.
65 of the tissue microenvironment to subsequent allergic responses.
66 velopment of the full spectrum of intestinal allergic responses.
67 ion is critical for the development of acute allergic responses.
68 that CD8 T cells can both prevent and cause allergic responses.
69 and their skin was tested for cross-reactive allergic responses.
70 h are important effector cells in immune and allergic responses.
71 ns as a critical negative regulator to limit allergic responses.
72 l, viral, and fungal infections and in acute allergic responses.
73 es, extending beyond the regulation of acute allergic responses.
74 erminal centers and in the effector phase of allergic responses.
75 nd in Th2 cytokine production in established allergic responses.
76 tumors or pathogens, or dampen autoimmune or allergic responses.
77 , including parasite infections, cancer, and allergic responses.
78 ctive mediators induced by allergens elicits allergic responses.
79 t cells that contributes to inflammatory and allergic responses.
80 nducible Foxp3 expression and the control of allergic responses.
81 L-13-producing CD4(+) T cells mediating lung allergic responses.
82 irst direct evidence that nicotine modulates allergic responses.
83 ukotriene C(4) (LTC(4)), which contribute to allergic responses.
84 flammatory signaling, alleviating T(H)2-type allergic responses.
85 pe 2 immunity, which drives a broad array of allergic responses.
86 me pathogenic effector cells, enhancing lung allergic responses.
87 E structure and renders it unable to mediate allergic responses.
88 ce to further dissect tissue lymphocytes and allergic responses.
89 on IgE can be a potential target to inhibit allergic responses.
90 velopment of allergen-specific inhibitors of allergic responses.
91 ereby interfering with its ability to induce allergic responses.
92 ard infusion-related adverse effects such as allergic responses.
93 C2s) can also contribute to orchestration of allergic responses.
94 n part of the strong psychological impact on allergic responses.
95 of allergen-specific IgE that is central to allergic responses.
96 of targeting miR-19 to alleviate pathogenic allergic responses.
97 ight be a mechanism to suppress IgE-mediated allergic responses.
98 e of both high and low affinity epitopes for allergic responses.
99 lease, and forestalling initiation of type 2 allergic responses.
100 in Results: DBP exposure increased the early allergic response (21.4% decline in FEV(1) area under th
102 one of the most popular foods in the world, allergic responses after ingesting pizza are relatively
104 Shedding light on the crosstalk between allergic response and cancer is paving the way for new a
105 suggests that a subset of ENMs may elicit an allergic response and contribute to the exacerbation of
106 tized to wheat proteins to induce a systemic allergic response and orally exposed to the same allerge
107 ILC2s have functional defects in the innate allergic response and represent a tool for studying inna
108 xes can be actively dissociated to block the allergic response and suggest that protein-protein compl
109 to study the molecules' ability to induce an allergic response and whether they induce allergen-speci
110 earch has not revealed how they initiate the allergic response and why the myriad of other inhaled pr
111 the effect of mast cell recruitment on acute allergic responses and (2) to define the role of phospho
115 expert groups focus on the interface between allergic responses and cancer, applied to immune surveil
116 cytokines IL-13 and IL-4 are produced during allergic responses and cause increases in airway epithel
117 hemical challenges through AhR by modulating allergic responses and contributing to the generation of
118 the development of peanut-induced intestinal allergic responses and for prevention and treatment of p
119 Geha, they studied the role of Th2 cells in allergic responses and he began work in Kawasaki's disea
121 l restoration of suppression of in vivo lung allergic responses and in vitro proliferation of activat
122 s, such as M pneumoniae, can augment ongoing allergic responses and inhibit pulmonary type 2 cytokine
124 atopic march from skin sensitization to food allergic responses and provide a model system for the ge
125 red hallmarks of eosinophil participation in allergic responses and related inflammatory reactions; h
126 ays a significant role in the development of allergic responses and sensitivities, but the mechanisms
127 andin (PG) D(2) is substantially involved in allergic responses and signals through the 7 transmembra
128 omplex/FcepsilonRII/Syk/IFN-gamma pathway in allergic responses and suggest that FcepsilonRII may pla
129 the exact mechanisms of their involvement in allergic responses and Th2 cell differentiation have rem
130 ed that SP-D-deficient mice exhibit enhanced allergic responses and that SP-D induction requires lymp
131 quired for cellular and humoral Th2-mediated allergic responses and the development of airway hyperre
132 sed to investigate the pathogenesis of human allergic responses and to test new therapeutics before t
133 s from CD8(-/-) mice failed to suppress lung allergic responses and were characterized by reduced lev
134 between exposure to HDM, development of the allergic response, and pathologic consequences in patien
135 nticancer therapies, modulate autoimmune and allergic responses, and prevent transplant rejection.
137 urring Foxp3(+)CD4(+)CD25(+) T cells on lung allergic responses are Ag-nonspecific and thus, independ
141 t have important roles in the development of allergic responses as well as the body of evidence on en
143 importance of T helper type 2 (T(H)2)-driven allergic responses, as well as of the non-allergic and i
144 HFD-induced obesity potentiates food-induced allergic responses associated with dysregulated intestin
145 ability to induce allergic inflammation and allergic responses but induced similar T-cell proliferat
146 ence identifies histamine as a key player in allergic responses, but the reports relating serum hista
147 hoid cells (ILC2s) modulate inflammatory and allergic responses, but their function in cancer immunit
148 to pathogenic effector cells, enhancing lung allergic responses, but these effects were mediated thro
149 d a week earlier is sufficient to trigger an allergic response-but only if participants had slept aft
150 IL-4 secretion by ILC2s contributes to the allergic response by reducing allergen-specific Treg cel
151 ition during allergic sensitization augments allergic responses by enhancing Th2 cell activation and
152 ls are integral to the development of airway allergic responses by modulating chemokine and/or cytoki
153 ut of HDM allergens showed an attenuation of allergic responses by targeting just a single component,
154 the pathways leading to enhancement of lung allergic responses by transferred nTreg and iTreg cells
158 with allergic rhinitis and appears to reduce allergic responses clinically and immunologically after
159 Many forms of hypersensitivity reactions and allergic responses depend on deregulated mast cell activ
161 to the steroid, dexamethasone, could inhibit allergic responses during the later stages of the diseas
162 and basophils, with release of agents of the allergic response, ensues when multivalent antigens bind
163 ndings demonstrate that Th2 cell-predominant allergic responses followed by immune phenotype switchin
165 T cells, developed the full spectrum of lung allergic responses following reconstitution with highly
166 Esophagitis, whether caused by acid reflux, allergic responses, graft-versus-host disease, drugs, or
167 istamines, which treat the symptoms after an allergic response has taken place; steroids, which resul
169 Recruitment of APC and TC to the lung during allergic responses has been demonstrated, but functional
170 ction, the role of RasGRP4 in mast cells and allergic responses has not been clearly demonstrated.
172 ng TH2 effector activation in the late-phase allergic response, IL-10 is a known IgG1 switch factor.
173 these two epitopes completely abrogated the allergic response in 14 of the 16 patients in an in vitr
177 ice were sufficient to confer an exaggerated allergic response in OVA-challenged WT mice, although ai
178 nical interest, as it has been implicated in allergic response in patients receiving therapeutic anti
179 nding was consistent with the lack of a full allergic response in SphK2-null mice challenged to under
180 allergic rhinitis (LAR) is a localized nasal allergic response in the absence of systemic atopy chara
181 reatment with butyrate significantly reduced allergic response in three animal models of FA, with a s
182 t CO(2) levels elicit a stronger RWE-induced allergic response in vivo and in vitro and that RWE incr
189 gen attenuated the sensitizing potential and allergic responses in Balb/c mice significantly and coul
196 1P and S1PR2 to MC- and IgE-dependent airway allergic responses in mice within minutes after antigen
197 adaptive humoral immune systems and modulate allergic responses in opposite directions, with sCD23 en
198 hts the importance of these cells for innate allergic responses in otherwise immunocompetent mice.
200 /-)and JNK2(-/-) mice failed to enhance lung allergic responses in sensitized and challenged CD8(-/-)
201 ted under hypoxic conditioning restored lung allergic responses in sensitized and challenged CD8-defi
209 Eos) are the major inflammatory component of allergic responses in the lungs of active asthmatics.
210 en associated with the induction of Th2-type allergic responses in the lungs, is also expressed in hu
212 uence of IgE on mast cell homeostasis during allergic responses in vivo has not been established.
217 ransferred into CD8-deficient mice, and lung allergic responses, including airway hyperresponsiveness
218 ted and selective inhibition of IgE-mediated allergic responses, including food, environmental, and d
219 zed mice resulted in a dramatic reduction of allergic response, indicating the role of B cells in amp
220 tribution of the IL-33/ST2 signaling axis in allergic responses induced by bacterial allergens are di
221 exert strongly suppressive functions toward allergic responses induced by naive and in vivo-primed h
222 these compounds have been reported to induce allergic responses, inflammatory responses, or no respon
223 tudy, we humanized three parent low affinity allergic response inhibitor (LARI) mouse anti-human IgE
224 mpletely changed the paradigms of allergy as allergic response is directed against an oligosaccharide
225 al urban environment of Singapore, where the allergic response is dominated by a single allergen (hou
228 ry cell (nTreg)-mediated suppression of lung allergic responses is abrogated following ligation of gl
232 In order for a protein to elicit a systemic allergic response it must reach the circulatory system t
233 ns with a focus on the role of basophils for allergic responses like asthma, allergic skin diseases a
234 wild-type mice, iTreg cells suppressed lung allergic responses linked to Smad3-dependent forkhead bo
236 us propose a dual role for MALT1 protease in allergic response, mediating 1) IgE-dependent mast cell
237 e whether loss of Stard7 expression promotes allergic responses, mice were generated in which one all
239 udy we sought to determine if exposure to an allergic response of the pregnant female in utero would
240 h DCs participate specifically in initiating allergic responses, particularly those associated with a
241 rovide an effective therapeutic strategy for allergic responses, particularly those involving interac
242 inducing an immediate Type I (IgE-mediated) allergic response, proteins intended for use in consumer
243 their well-established role as regulators of allergic response, recent evidence supports a role for m
244 l functions have classically been related to allergic responses, recent studies indicate that these c
246 ls (nTregs) resulting in suppression of lung allergic responses requires interaction of MHC class I o
249 eading to initiation and exacerbation of the allergic response that might have implications for desig
250 o induce susceptibility to the inappropriate allergic responses that characterize atopy and asthma.
251 terobivalent inhibitor (HBI) of IgE-mediated allergic responses that selectively inhibits allergen-Ig
253 l compounds to control the initiation of the allergic response through engagement of innate immunity.
254 n test (BAT) has become a pervasive test for allergic response through the development of flow cytome
257 of peanut allergy, regulating peanut-induced allergic responses through effects on steroidogenesis, a
258 e postulated that SP-D may decrease adaptive allergic responses through interaction with T cells.
259 IgE has a key role in the pathogenesis of allergic responses through its ability to activate mast
260 +) T regulatory cells (nTregs) regulate lung allergic responses through production of IL-10 and TGF-b
261 Mast cells are known for their roles in allergic responses, thus in this study we sought to dete
263 erapy can be used experimentally to treat an allergic response to another allergen and that the molec
264 common scientific name used to describe the allergic response to attacks in humans from nonspecific
266 hese data demonstrate that IL-23 dampens the allergic response to cryptococcal infection through IL-1
271 eled and is based on initiation of a type II allergic response to specific food antigens, leading to
272 gatively charged silica (20 nm) NPs suppress allergic response to two chemically distinct sensitizers
273 ide immunotherapy can be exploited to reduce allergic responses to a second allergen, ovalbumin (OVA)
275 estinal bacteria are critical for regulating allergic responses to dietary antigens and suggest that
276 with global WASP deficiency, indicating that allergic responses to food allergens are dependent upon
285 B cells, play a pivotal role in suppressing allergic responses to inhaled, ingested and injected all
286 tor for FLA, was required for priming strong allergic responses to natural indoor allergens present i
288 envenomation and initiates inflammatory and allergic responses to venoms remain largely unknown.
293 rienes (cysLTs) are also produced during the allergic response, we investigated the possibility that
294 rs (IL-13 levels, eosinophil numbers) of the allergic response were assessed in bronchoalveolar lavag
298 ial to modulate the elicitation phase of the allergic response which depends on the NP charge and com
299 mice enhanced the development of these lung allergic responses, which was reversed by exogenous IFN-