ライフサイエンスコーパス: allergic response

1 importance of B cells in maintenance of the allergic response.

2 se are downregulated by Th2 cytokines of the allergic response.

3 r activation of the immune system during the allergic response.

4 development of Th2 cells and the subsequent allergic response.

5 nse to TSLP by CD4 T cells in vivo during an allergic response.

6 T mice, which did not exhibit an OVA-induced allergic response.

7 resentation, and (may) thereby influence the allergic response.

8 ature coincident with the suppression of the allergic response.

9 exercise-induced asthma, and the late-phase allergic response.

10 itical role in the development of Brazil nut-allergic response.

11 ing sensitization and challenge phases of an allergic response.

12 mast cells and basophils in the food-induced allergic response.

13 ls, and trigger inflammatory cascades of the allergic response.

14 te inflammatory pathways associated with the allergic response.

15 play pivotal roles in the initiation of the allergic response.

16 f the possible development of the late-phase allergic response.

17 ophils and eosinophils during the late-phase allergic response.

18 helicidin before sensitization inhibited the allergic response.

19 f the fungal infection and prevention of the allergic response.

20 the release of mediators of the early phase allergic response.

21 ipate in the induction and regulation of the allergic response.

22 from cells is considered a key event in the allergic response.

23 IgE, the antibody isotype that mediates the allergic response.

24 at IL-10 is not the primary modulator of the allergic response.

25 leased by mast cells induce and maintain the allergic response.

26 in conjunctival tissue during an OVA-induced allergic response.

27 ucosal tissue that results in the late-phase allergic response.

28 ntibodies were the effector molecules of the allergic response.

29 s of mice undergoing house dust mite-induced allergic response.

30 signaling pathways in the initiation of the allergic response.

31 poietin secretion and a cutaneous T-helper 2 allergic response.

32 possibly having a role in IgG modulation of allergic response.

33 (TSLP) secretion and a cutaneous T-helper 2 allergic response.

34 CFP to allergic recipients downmodulated the allergic response.

35 tes mast cells and basophils, initiating the allergic response.

36 thought to play a role in the development of allergic responses.

37 Mast cells play critical roles in allergic responses.

38 's critical involvement in the regulation of allergic responses.

39 D25(+) T cells, enhanced development of lung allergic responses.

40 xploited therapeutically for modification of allergic responses.

41 supports its role as a mediator of immediate allergic responses.

42 DC migration and subsequent modification of allergic responses.

43 n CD4(+) T cells showed markedly ameliorated allergic responses.

44 exogenous stimulation and may contribute to allergic responses.

45 of allergen-specific IgE that is central to allergic responses.

46 modulating adaptive immunity during chronic allergic responses.

47 major allergen and is responsible for severe allergic responses.

48 inase (PI3K) isoforms in sequential steps to allergic responses.

49 STAT6 plays a central role in IL-4-mediated allergic responses.

50 nsitization and whether recruitment promotes allergic responses.

51 e molecular interactions taking place during allergic responses.

52 hat has been implicated in the initiation of allergic responses.

53 is a costimulatory molecule involved in Th2 allergic responses.

54 otential proresolving therapeutic agents for allergic responses.

55 ng contributes to the effector phase of some allergic responses.

56 of the tissue microenvironment to subsequent allergic responses.

57 velopment of the full spectrum of intestinal allergic responses.

58 ion is critical for the development of acute allergic responses.

59 that CD8 T cells can both prevent and cause allergic responses.

60 and their skin was tested for cross-reactive allergic responses.

61 h are important effector cells in immune and allergic responses.

62 ns as a critical negative regulator to limit allergic responses.

63 l, viral, and fungal infections and in acute allergic responses.

64 es, extending beyond the regulation of acute allergic responses.

65 nd in Th2 cytokine production in established allergic responses.

66 tumors or pathogens, or dampen autoimmune or allergic responses.

67 , including parasite infections, cancer, and allergic responses.

68 ctive mediators induced by allergens elicits allergic responses.

69 t cells that contributes to inflammatory and allergic responses.

70 nducible Foxp3 expression and the control of allergic responses.

71 L-13-producing CD4(+) T cells mediating lung allergic responses.

72 irst direct evidence that nicotine modulates allergic responses.

73 ukotriene C(4) (LTC(4)), which contribute to allergic responses.

74 exposure may increase the risk of developing allergic responses.

75 hat is essential for mast cell signaling and allergic responses.

76 hma and found that CD45RB ligation decreases allergic responses.

77 of targeting miR-19 to alleviate pathogenic allergic responses.

78 ry syncytial viral infection and OVA-induced allergic responses.

79 ex is dedicated to immunoglobulin E-mediated allergic responses.

80 vestigate the role of histamine in pulmonary allergic responses.

81 tors that reduce SHS and DEP exacerbation of allergic responses.

82 CXCL1, in airway walls resulted in worsened allergic responses.

83 esponses and thereby reducing autoimmune and allergic responses.

84 to allergen immunotherapy that reduces acute allergic responses.

85 before OVA aerosol challenge also prevented allergic responses.

86 e of both high and low affinity epitopes for allergic responses.

87 lease, and forestalling initiation of type 2 allergic responses.

88 attempted to prenatally abolish or diminish allergic responses.

89 ipients fails to restore development of lung allergic responses.

90 demonstrated to contribute to modulation of allergic responses.

91 p110delta-selective inhibitor idelalisib on allergic responses.

92 relating ozone to respiratory infections and allergic responses.

93 ard infusion-related adverse effects such as allergic responses.

94 Mast cells play an important role in allergic responses.

95 often leads to T helper 2 (Th2) cell-driven allergic responses.

96 ongylus brasiliensis to induce innate type 2 allergic responses.

97 resident Th2 memory cells as drivers of lung allergic responses.

98 that can both promote and curb Th2-dependent allergic responses.

99 C2s) can also contribute to orchestration of allergic responses.

100 t to function as an adjuvant that can induce allergic responses.

101 ling in Th2 cytokine-driven inflammation and allergic responses.

102 immunomodulatory properties of histamine in allergic responses.

103 ophils, which contribute to the pathology of allergic responses.

104 IgE, the antibody that mediates allergic responses, acts as part of a self-regulating pr

105 Shedding light on the crosstalk between allergic response and cancer is paving the way for new a

106 suggests that a subset of ENMs may elicit an allergic response and contribute to the exacerbation of

107 (FcepsilonRI) is a central component of the allergic response and is expressed as either a trimeric

108 E receptor, is an important modulator of the allergic response and of diseases such as rheumatoid art

109 tized to wheat proteins to induce a systemic allergic response and orally exposed to the same allerge

110 ILC2s have functional defects in the innate allergic response and represent a tool for studying inna

111 xes can be actively dissociated to block the allergic response and suggest that protein-protein compl

112 to study the molecules' ability to induce an allergic response and whether they induce allergen-speci

113 earch has not revealed how they initiate the allergic response and why the myriad of other inhaled pr

114 the effect of mast cell recruitment on acute allergic responses and (2) to define the role of phospho

115 but also had therapeutic effects on systemic allergic responses and airway hyperresponsiveness.

116 monary C. neoformans infection to potentiate allergic responses and airway reactivity and suggest a p

117 ntial for pulmonary cryptococcosis to modify allergic responses and airway reactivity.

118 r role in human diseases beyond IgE-mediated allergic responses and antiparasitic functions.

119 expert groups focus on the interface between allergic responses and cancer, applied to immune surveil

120 cytokines IL-13 and IL-4 are produced during allergic responses and cause increases in airway epithel

121 hemical challenges through AhR by modulating allergic responses and contributing to the generation of

122 X) metabolic pathway is actively involved in allergic responses and COX inhibition increases allergic

123 the development of peanut-induced intestinal allergic responses and for prevention and treatment of p

124 t by T helper 2 (Th2) cytokines that mediate allergic responses and IgE production.

125 l restoration of suppression of in vivo lung allergic responses and in vitro proliferation of activat

126 the cytokine activin-A suppress TH2-mediated allergic responses and linked airway disease.

127 atopic march from skin sensitization to food allergic responses and provide a model system for the ge

128 andin (PG) D(2) is substantially involved in allergic responses and signals through the 7 transmembra

129 omplex/FcepsilonRII/Syk/IFN-gamma pathway in allergic responses and suggest that FcepsilonRII may pla

130 the exact mechanisms of their involvement in allergic responses and Th2 cell differentiation have rem

131 ed that SP-D-deficient mice exhibit enhanced allergic responses and that SP-D induction requires lymp

132 quired for cellular and humoral Th2-mediated allergic responses and the development of airway hyperre

133 sed to investigate the pathogenesis of human allergic responses and to test new therapeutics before t

134 s from CD8(-/-) mice failed to suppress lung allergic responses and were characterized by reduced lev

135 between exposure to HDM, development of the allergic response, and pathologic consequences in patien

136 nticancer therapies, modulate autoimmune and allergic responses, and prevent transplant rejection.

137 ribute to protective immunity, inappropriate allergic responses, and tissue repair.

138 urring Foxp3(+)CD4(+)CD25(+) T cells on lung allergic responses are Ag-nonspecific and thus, independ

139 We review the myriad ways in which HDM allergic responses are orchestrated.

140 ollen lipids by iNKT cells and their role in allergic responses are poorly defined.

141 e also involved in autoimmunity, asthma, and allergic responses as well as in tumor immunity.

142 Transfer of nTreg cells enhanced lung allergic responses, as did transfer of iTreg cells.

143 importance of T helper type 2 (T(H)2)-driven allergic responses, as well as of the non-allergic and i

144 ability to induce allergic inflammation and allergic responses but induced similar T-cell proliferat

145 ence identifies histamine as a key player in allergic responses, but the reports relating serum hista

146 hoid cells (ILC2s) modulate inflammatory and allergic responses, but their function in cancer immunit

147 to pathogenic effector cells, enhancing lung allergic responses, but these effects were mediated thro

148 acts as a novel epithelial regulator of the allergic response by altering Th2 cell recruitment and e

149 IL-4 secretion by ILC2s contributes to the allergic response by reducing allergen-specific Treg cel

150 ition during allergic sensitization augments allergic responses by enhancing Th2 cell activation and

151 ls are integral to the development of airway allergic responses by modulating chemokine and/or cytoki

152 Here we show that RGS13 inhibited allergic responses by physically interacting with the re

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

155 Thus, inhibition by ISS of allergic responses can be explained by two novel mechani

156 Allergic responses can be triggered by structurally dive

157 with allergic rhinitis and appears to reduce allergic responses clinically and immunologically after

158 Recent work further characterizes the allergic response, demonstrating a population of eosinop

159 Many forms of hypersensitivity reactions and allergic responses depend on deregulated mast cell activ

160 ensitization affects the airway and systemic allergic response differently.

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

164 b(-/-) mice were generated and exhibit hyper-allergic responses following antigen challenge.

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

168 Although a role in pathogen and allergic responses has been assigned to the RORgammat(+)

169 Recruitment of APC and TC to the lung during allergic responses has been demonstrated, but functional

170 A significant role for PGD2 in mediating allergic responses has been suggested based on the obser

171 ction, the role of RasGRP4 in mast cells and allergic responses has not been clearly demonstrated.

172 TH2 differentiation and development of lung allergic responses has not been investigated.

173 ng TH2 effector activation in the late-phase allergic response, IL-10 is a known IgG1 switch factor.

174 e effect of endotoxin in bedding dust on the allergic response in HDM-sensitised individuals.

175 re the impact of T reg cell depletion on the allergic response in mice susceptible (A/J) or comparati

176 ice were sufficient to confer an exaggerated allergic response in OVA-challenged WT mice, although ai

177 nical interest, as it has been implicated in allergic response in patients receiving therapeutic anti

178 nding was consistent with the lack of a full allergic response in SphK2-null mice challenged to under

179 allergic rhinitis (LAR) is a localized nasal allergic response in the absence of systemic atopy chara

180 1 (H1R) and H4 receptors (H4R) in intestinal allergic responses in a model of peanut allergy.

181 mine whether IL-15(-/-) mice have attenuated allergic responses in a mouse model of AAD.

182 While DEP is known to augment allergic responses in adult animal models, its effects o

183 D25(+) T cells as capable of regulating lung allergic responses in an IL-10- and TGF-beta-dependent m

184 port that IL-15(-/-) mice developed enhanced allergic responses in an OVA-induced model of AAD.

185 ole for CD206 in regulating allergen induced allergic responses in asthma.

186 gen attenuated the sensitizing potential and allergic responses in Balb/c mice significantly and coul

187 7BL/6 mice, the infection did not reduce the allergic responses in BALB/c mice.

188 ired for T helper type 2 (TH2), but not TH1, allergic responses in both the skin and lungs.

189 Clinical evidence implicating mucosal allergic responses in dysmotility has been extended to i

190 om Postn(+/+) mice was sufficient to promote allergic responses in F6 Postn(-/-) littermates.

191 Mast cells are a critical component of allergic responses in humans, and animal models that all

192 Increased airway allergic responses in Map3k8(-/-) mice were not due to a

193 1P and S1PR2 to MC- and IgE-dependent airway allergic responses in mice within minutes after antigen

194 adaptive humoral immune systems and modulate allergic responses in opposite directions, with sCD23 en

195 hts the importance of these cells for innate allergic responses in otherwise immunocompetent mice.

196 erized for its role during the initiation of allergic responses in peripheral tissues.

197 /-)and JNK2(-/-) mice failed to enhance lung allergic responses in sensitized and challenged CD8(-/-)

198 nvestigate how nanoparticles (NPs) may alter allergic responses in skin.

199 the design topical therapeutics to mitigate allergic responses in skin.

200 The effects of IL-33 on allergic responses in the airways of sensitized mice wer

201 However, its relevance for the modulation of allergic responses in the lung remains unclear.

202 Enhanced allergic responses in the lung were accompanied by age-d

203 nin pathway in the DC-mediated regulation of allergic responses in the lung.

204 y in the development of CD8+ T cell-mediated allergic responses in the lung.

205 nal nematodes but is largely dispensable for allergic responses in the lung.

206 Eos) are the major inflammatory component of allergic responses in the lungs of active asthmatics.

207 en associated with the induction of Th2-type allergic responses in the lungs, is also expressed in hu

208 ng and to correlate these changes to chronic allergic responses in tissue.

209 uence of IgE on mast cell homeostasis during allergic responses in vivo has not been established.

210 Abs in promoting mast cell expansion during allergic responses in vivo.

211 ne in the development of inflammatory and/or allergic responses in vivo.

212 Systemic exacerbation of allergic responses, in which mast cells play a critical

213 interleukin-13 and hallmark features of the allergic response including airway hyperreactivity.

214 ted and selective inhibition of IgE-mediated allergic responses, including food, environmental, and d

215 zed mice resulted in a dramatic reduction of allergic response, indicating the role of B cells in amp

216 exert strongly suppressive functions toward allergic responses induced by naive and in vivo-primed h

217 these compounds have been reported to induce allergic responses, inflammatory responses, or no respon

218 al urban environment of Singapore, where the allergic response is dominated by a single allergen (hou

219 In a tropical urban environment, the allergic response is dominated by a single allergen clas

220 The allergic response is initiated on the plasma membrane of

221 ry cell (nTreg)-mediated suppression of lung allergic responses is abrogated following ligation of gl

222 While the role of IgE in mediating allergic responses is best described on basophils and ma

223 ultimately mediates said innate and adaptive allergic responses is poorly understood.

224 In order for a protein to elicit a systemic allergic response it must reach the circulatory system t

225 ns with a focus on the role of basophils for allergic responses like asthma, allergic skin diseases a

226 mulating evidence demonstrating that mucosal allergic responses may disrupt gut motility, and may als

227 There is also evidence that mucosal allergic responses may induce long-term changes in visce

228 Conceptually, allergic responses may involve cross-reactivity by antib

229 e whether loss of Stard7 expression promotes allergic responses, mice were generated in which one all

230 Consequently we studied the allergic response of Fe(III) complex of the protein frac

231 gested a negative feedback loop, controlling allergic responses of eosinophils and helper T cells, vi

232 ation pathway for fibroblasts during chronic allergic responses on interaction with recruited eosinop

233 h DCs participate specifically in initiating allergic responses, particularly those associated with a

234 rovide an effective therapeutic strategy for allergic responses, particularly those involving interac

235 their well-established role as regulators of allergic response, recent evidence supports a role for m

236 l functions have classically been related to allergic responses, recent studies indicate that these c

237 e induction in Th2 cells and its relation to allergic responses remain unclear.

238 and the genetic etiology for differences in allergic responses remain unclear.

239 ls (nTregs) resulting in suppression of lung allergic responses requires interaction of MHC class I o

240 Functionally, T(H)9 cells promote allergic responses resulting in enhanced pathology media

241 nal antibody GK1.5 on the development of the allergic responses seen during active fungal infection.

242 The relative attenuation of allergic responses seen in C57BL/6 mice was dependent on

243 Allergic responses, serological antibody levels, intesti

244 ulmonary fungal infection accompanied by an "allergic" response (T2) to the infection, i.e., a model

245 eading to initiation and exacerbation of the allergic response that might have implications for desig

246 o induce susceptibility to the inappropriate allergic responses that characterize atopy and asthma.

247 terobivalent inhibitor (HBI) of IgE-mediated allergic responses that selectively inhibits allergen-Ig

248 In the OVA-induced allergic response, the numbers of conjunctival mast cell

249 l compounds to control the initiation of the allergic response through engagement of innate immunity.

250 n test (BAT) has become a pervasive test for allergic response through the development of flow cytome

251 ty, play a role in the initiation of the HDM-allergic response through TLR2 activation.

252 Mast cells elicit allergic responses through degranulation and release of

253 IgG and FcgammaRIIb suppress adaptive allergic responses through effects on mast cell function

254 of peanut allergy, regulating peanut-induced allergic responses through effects on steroidogenesis, a

255 es (DEPs) can initiate and exacerbate airway allergic responses through enhanced IgE production.

256 e postulated that SP-D may decrease adaptive allergic responses through interaction with T cells.

257 IgE has a key role in the pathogenesis of allergic responses through its ability to activate mast

258 +) T regulatory cells (nTregs) regulate lung allergic responses through production of IL-10 and TGF-b

259 hts their likely important role in the early allergic response to aeroallergens in the airways.

260 thelial cells; and stimulated the subsequent allergic response to Ag challenge.

261 common scientific name used to describe the allergic response to attacks in humans from nonspecific

262 ion, the inflammasome is dispensable for the allergic response to bee venom.

263 IFN-gamma, C57BL/6 mice develop an augmented allergic response to C. neoformans, including enhanced g

264 hese data demonstrate that IL-23 dampens the allergic response to cryptococcal infection through IL-1

265 ation of skin DCs to DLNs and the subsequent allergic response to e.c. introduced antigen.

266 hildren is reported to be associated with an allergic response to food antigens.

267 The allergic response to HDMs is partially mediated by epith

268 Allergic response to pollen is increasing worldwide, lea

269 ich fungal colonization is accompanied by an allergic response to the fungus.

270 gatively charged silica (20 nm) NPs suppress allergic response to two chemically distinct sensitizers

271 with global WASP deficiency, indicating that allergic responses to food allergens are dependent upon

272 ate mechanisms underlying persistent IgE and allergic responses to food allergens.

273 ering IL-25 signaling enhances or attenuates allergic responses to food allergens.

274 ls leads to release of MMP-9 which decreases allergic responses to GC frass.

275 Blockade of OX40L significantly lessened allergic responses to HDM or peanut.

276 and radiosensitive cells in the lung promote allergic responses to HDMs.

277 allergic asthma by TLR5-dependent priming of allergic responses to indoor allergens.

278 fic DNAzyme attenuated early- and late-phase allergic responses to inhaled allergen.

279 B cells, play a pivotal role in suppressing allergic responses to inhaled, ingested and injected all

280 tor for FLA, was required for priming strong allergic responses to natural indoor allergens present i

281 t not disseminated infection) can exacerbate allergic responses to respiratory challenge with ovalbum

282 W/chronic infection provided protection from allergic responses to RW with significantly fewer eosino

283 ants (Ile105 and Val105) are determinants of allergic responses to SHS, and that responses to SHS and

284 ice acts in two distinct ways to prevent the allergic responses to this challenge.

285 envenomation and initiates inflammatory and allergic responses to venoms remain largely unknown.

286 oral immunotherapy is effective in reducing allergic responses towards shrimp tropomyosin.

287 e first identifiable biochemical step of the allergic response, under the same conditions.

288 This work suggests that the H4R can modulate allergic responses via its influence on T cell activatio

289 Initially, the Th2-biased HDM allergic response was considered to be mediated only by

290 Oral tolerance to the Th2 allergic response was in large part dependent on TGF-bet

291 Enhancement of lung allergic responses was accompanied by reduced expression

292 Infection-associated enhancement of allergic responses was not dependent on cryptococcal enc

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

295 These allergic responses were dependent on subtilisin protease

296 Local and systemic allergic responses were evaluated.

297 to the RSV-induced airway attenuation of the allergic responses, whereas transfer of CD8 T cells from

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-

300 notherapy holds the potential for modulating allergic responses without IgE cross-linking.