ライフサイエンスコーパス: anaphylaxis

1 dditional lower steps for index reactions of anaphylaxis).

2 d anaphylaxis without affecting IgE-mediated anaphylaxis.

3 silonRI/mast cells in promoting IgE-mediated anaphylaxis.

4 ce were orally challenged with OVA to induce anaphylaxis.

5 r year in the incidence rate of food-related anaphylaxis.

6 61 was assessed for its ability to influence anaphylaxis.

7 , including rash, fever, serum sickness, and anaphylaxis.

8 ing intact K9.36 suppression of IgG-mediated anaphylaxis.

9 ne of the most common causes of food-related anaphylaxis.

10 erial infections can alter susceptibility to anaphylaxis.

11 at EPIT induced sustained protection against anaphylaxis.

12 ation-based epidemiologic data collection on anaphylaxis.

13 and was significantly associated with severe anaphylaxis.

14 aRIIB to negatively regulate these models of anaphylaxis.

15 axis without strongly affecting IgE-mediated anaphylaxis.

16 in in the albedo of Citrus unshiu may induce anaphylaxis.

17 65% of these were subsequently classified as anaphylaxis.

18 oderate NPV and sensitivity in perioperative anaphylaxis.

19 sing serum total mast cell tryptase (MCT) in anaphylaxis.

20 fication and classification of patients with anaphylaxis.

21 alloantibody to mouse FcgammaRIIB, on murine anaphylaxis.

22 eat, all patients had no further episodes of anaphylaxis.

23 ight influence the occurrence or severity of anaphylaxis.

24 ll emergency visits in adults presented with anaphylaxis.

25 nd were significantly associated with severe anaphylaxis.

26 nti-FcgammaRIIB safely prevents IgG-mediated anaphylaxis.

27 ild, involving mainly the skin, and, rarely, anaphylaxis.

28 phylaxis of unknown cause and 27% deemed non-anaphylaxis.

29 toms, preventing and protecting them against anaphylaxis.

30 te to severe with a risk of life-threatening anaphylaxis.

31 l for studying food allergy and IgE-mediated anaphylaxis.

32 iteria were based on the Sampson criteria of anaphylaxis.

33 (DC)(-/-) mice are resistant to IgE-mediated anaphylaxis.

34 IgG2a-, and IgG2b-dependent passive systemic anaphylaxis.

35 all-molecule inhibition of STAT3 can prevent anaphylaxis.

36 effector phase of peanut-induced intestinal anaphylaxis.

37 as evaluated on these cells before and after anaphylaxis.

38 of the St. Pierre hospital in Brussels with anaphylaxis.

39 ed to competence in recognizing and managing anaphylaxis.

40 sensitive to IgE-mediated, passive, systemic anaphylaxis.

41 patients with allergic diseases and to fatal anaphylaxis.

42 utaneous tolerance can suppress food-induced anaphylaxis.

43 e been shown to enable induction of systemic anaphylaxis.

44 There were no reports of fatal anaphylaxis.

45 protected the mice from severe IgE-mediated anaphylaxis.

46 plicated in food-dependent, exercise-induced anaphylaxis.

47 s, and macrophages to IgG subclass-dependent anaphylaxis.

48 present as Hymenoptera-induced or idiopathic anaphylaxis.

49 ivo and in a mouse model of passive systemic anaphylaxis.

50 unotherapy (EPIT) in a model of food-induced anaphylaxis.

51 syndromes, including angioedema or systemic anaphylaxis.

52 evere atopic disease, including food-induced anaphylaxis.

53 or basophils in the pathophysiology of human anaphylaxis.

54 nificantly associated only with food-induced anaphylaxis.

55 gy rather than simply increased reporting of anaphylaxis.

56 er basophils have an important role in human anaphylaxis.

57 gE-mediated anaphylaxis, 2% non-IgE-mediated anaphylaxis, 12% anaphylaxis of unknown cause and 27% de

58 Aetiology included 59% IgE-mediated anaphylaxis, 2% non-IgE-mediated anaphylaxis, 12% anaphy

59 had histories of urticaria/angioedema, 50 of anaphylaxis, 26 of nonimmediate cutaneous eruptions, and

60 mice were susceptible to passive and active anaphylaxis, accompanied by downregulation of both activ

61 2 represents a useful composite biomarker of anaphylaxis, achieving superior diagnostic power over ei

62 (nonallergic, history of allergen-triggered anaphylaxis, acute cardiovascular/febrile reactions).

63 We calculated the incidence of anaphylaxis after all vaccines combined and for selected

64 y occasional exposures; however, no cases of anaphylaxis after eating a Citrus unshiu, the albedo of

65 mediated MC degranulation, and promotes oral anaphylaxis after epicutaneous sensitization by targetin

66 travenous immunoglobulin and active systemic anaphylaxis after immunization and challenge.

67 with a jellyfish allergy due to IgE mediated anaphylaxis after ingestion.

68 The risk of anaphylaxis after vaccination has not been well describe

69 cine Safety Datalink, we determined rates of anaphylaxis after vaccination in children and adults.

70 ctose (alpha-gal) is known to induce delayed anaphylaxis against mammalian meat.

71 er the changes observed during venom-related anaphylaxis also occur during allergic reactions to food

72 data revealed fewer hospital attendances for anaphylaxis among non-Western immigrants compared to Dan

73 was available in 71 of 82 (87%) patients (60 anaphylaxis and 11 controls).

74 Anaphylaxis and allergic lung inflammation were restored

75 codes; 309 files (46%) from 209 patients had anaphylaxis and allergic or hypersensitivity comorbiditi

76 Although unable to discriminate between anaphylaxis and cardiovascular/febrile reactions, ROC cu

77 the mechanism by which STAT3 contributes to anaphylaxis and determine whether small-molecule inhibit

78 et the Brighton Collaboration definition for anaphylaxis and had to be determined to be vaccine trigg

79 ether with those of patients with idiopathic anaphylaxis and healthy control subjects (7 of each) wer

80 ion by the VE compartment in the severity of anaphylaxis and identify a new pathway for therapeutic i

81 apabilities of hFcgammaRs to induce systemic anaphylaxis and identify the cell types and mediators in

82 )(-/-) ) demonstrated a similar reduction in anaphylaxis and IgE.

83 Risk of anaphylaxis and implications for social activities affec

84 eatment option in SM, effectively preventing anaphylaxis and improving chronic MC mediator-related sy

85 ation should be performed, particularly when anaphylaxis and long interval to diagnosis are present.

86 , effector cells, or mediators implicated in anaphylaxis and mice that have been "humanized" for some

87 and a preclinical model of passive cutaneous anaphylaxis and passive systemic anaphylaxis that can be

88 e treatment was most effective for recurrent anaphylaxis and skin symptoms, less for gastrointestinal

89 alexithymia, followed by trait anxiety, age, anaphylaxis and social support.

90 ferent mechanisms as having a primal role in anaphylaxis and that IgE-dependent and distinct IgE-inde

91 s involved in these IgE-independent forms of anaphylaxis and the clinical evidence for their human re

92 s backgrounds in prevention and treatment of anaphylaxis and the close collaboration with allergologi

93 thinking, are younger, will have experienced anaphylaxis and will have lower social support.

94 to vaccination (one febrile reaction and one anaphylaxis) and one possibly related (influenza-like il

95 ty (73%) patients fulfilled WAO criteria for anaphylaxis, and 22 patients did not.

96 d mAbs present with nonclassical symptoms of anaphylaxis, and patients may present with unrecognized

97 or primarily responsible for all 3 models of anaphylaxis, and subsequent downregulation of this recep

98 e tolerance threshold, to reduce the risk of anaphylaxis, and to improve the patient's quality of lif

99 nsyl-specific IgE-mediated passive cutaneous anaphylaxis; and attenuate dansyl IgE-mediated systemic

100 or more of 11 potentially allergic diseases (anaphylaxis, angioedema, asthma, conjunctivitis, drug al

101 um difficile infections, and 2 to 6 cases of anaphylaxis annually.

102 ore, in a low-dose model of passive systemic anaphylaxis, antigen-dependent decrease in body temperat

103 Deaths from anaphylaxis are difficult to investigate because of misc

104 Most published studies on anaphylaxis are retrospective or register based.

105 ulted in reduced development and severity of anaphylaxis as measured by decline of body temperature,

106 , they exhibited mast-cell-mediated systemic anaphylaxis, as indicated by hypothermia and increases i

107 bacter pylori confers protection against the anaphylaxis associated with ovalbumin and peanut allergy

108 8 of the 124 fulfilled WAO/EAACI criteria of anaphylaxis at the ECS, while six were found among 46 pa

109 to characterize patients seen with suspected anaphylaxis at the emergency care setting (ECS), after s

110 igated variations in hospital attendance for anaphylaxis between immigrants and Danish-born including

111 deplete FcgammaRIII or suppress IgG-mediated anaphylaxis but prevented intact K9.361-induced anaphyla

112 ent's serum of previously reported enokitake anaphylaxis, but a 75kDa band showing specific reaction

113 ng to the EAACI guidelines for management of anaphylaxis, but only a minority received the recommende

114 (eg, certain foods or single insect stings), anaphylaxis can be considered the most aberrant example

115 Because IgG- and IgE-mediated anaphylaxis can be mediated by the same cell types, this

116 Anaphylaxis can proceed through distinct IgE- or IgG-dep

117 Possible anaphylaxis cases were daily identified based on a broad

118 ic and procedure codes to identify potential anaphylaxis cases.

119 Several reports have described anaphylaxis caused by the ingestion of jellyfish, but th

120 lower risk ratio of hospital attendance for anaphylaxis compared to Danish-born.

121 minance in mice with IgG1- and IgG2b-induced anaphylaxis correlated with the ability of inhibitory Fc

122 hern Europe cities, some cases of idiopathic anaphylaxis could potentially be caused by A. reflexus i

123 line in hemodynamically stable patients with anaphylaxis could prevent the development of hypotension

124 y database demonstrated undernotification of anaphylaxis deaths due, at least in part, to difficult c

125 We re-estimated the anaphylaxis deaths that occurred in Brazil during the pe

126 umber of cases; moreover, all 606 definitive anaphylaxis deaths would be considered as underlying cau

127 of which 95% were classified as 'definitive anaphylaxis deaths'.

128 We identified 639 anaphylaxis deaths, of which 95% were classified as 'def

129 pacity of the new ICD-11 revision to capture anaphylaxis deaths.

130 report in detail a case of severe nocturnal anaphylaxis due to pigeon tick bite showing the diagnost

131 o determine the incidence rate and causes of anaphylaxis during a 10-year period in Olmsted County, M

132 analyses of cases of suspected perioperative anaphylaxis during general anaesthesia (GA) were perform

133 ificant increase in the overall incidence of anaphylaxis during the study period, with an average inc

134 cat) and those that induce life-threatening anaphylaxis (e.g. Hymenoptera venom).

135 study, 10 of the 11 children with CM induced anaphylaxis enrolled in a CMA OIT clinical trial and com

136 95% CI, 7.2% to 12.2%) students reported 93 anaphylaxis episodes.

137 he F(ab')2 fragment of K9.361 did not induce anaphylaxis, even after beta-adrenergic blockade, and di

138 concerns that botulinum antitoxin can induce anaphylaxis exist.

139 Considering the <2 % rate of anaphylaxis, fatal outcomes, modest predictive value of

140 Food-dependent exercise-induced anaphylaxis (FDEIAn) was suspected.

141 he immunopathogenesis and pathophysiology of anaphylaxis, focusing on the roles of IgE and IgG antibo

142 ading to attenuated mast cell activation and anaphylaxis following FcvarepsilonRI cross-linking.

143 ystematically overestimate the risk of fatal anaphylaxis for a food allergic child.

144 fessionals accurately estimate risk of fatal anaphylaxis for food allergic children, and whether accu

145 ignificantly overestimated the risk of fatal anaphylaxis for food allergic children, by a mean factor

146 Finally, we will speculate about anaphylaxis from an evolutionary perspective and argue t

147 ying all first-time hospital attendances for anaphylaxis from January 1, 1994 and December 31, 2010.

148 cted by consensus equation was higher in the anaphylaxis group compared to controls (P=.0001).

149 Anaphylaxis has been defined as a 'severe, life-threaten

150 However, IgE-independent mechanisms of anaphylaxis have been clearly demonstrated in experiment

151 But some cases of anaphylaxis have been reported.

152 Rising rates of food-induced anaphylaxis have recently been shown in the adolescent a

153 iated meat allergy (MA) patients, idiopathic anaphylaxis (IA) patients with suspected MA, and non-mea

154 ants referred with a diagnosis of idiopathic anaphylaxis (IA), six (9%) were found to have IgE to alp

155 rders also occur in patients with idiopathic anaphylaxis (IA).

156 rsensitivity conditions, 673 had some of the anaphylaxis ICD-10 codes; 309 files (46%) from 209 patie

157 rinized IgG2a) can induce the development of anaphylaxis in C57BL/6 mice upon repeated i.p. dosing be

158 ; and attenuate dansyl IgE-mediated systemic anaphylaxis in human FcepsilonRIalpha transgenic mouse m

159 Evidence from studies of anaphylaxis in human subjects will be discussed, as well

160 Similarly, attenuated passive anaphylaxis in IL-10(-/-) mice could be restored by IL-1

161 Gal) is associated with IgE-mediated delayed anaphylaxis in meat allergy.

162 strated by the inability of IL-10 to enhance anaphylaxis in miR-155-deficient mice.

163 ion might be useful in treating food-induced anaphylaxis in patients with AD.

164 prophylactic induction of tolerance, induce anaphylaxis in presensitized mice.

165 pisode of anaphylaxis increased the risk for anaphylaxis in SCIT (OR [95% CI] = 17.35 [1.91-157.28],

166 the previously reported rise in food-induced anaphylaxis in this age group may reflect an increasing

167 Hymenoptera stings can cause severe anaphylaxis in untreated venom-allergic patients.

168 ranulation and efficiently inhibits systemic anaphylaxis in vivo.

169 erbated and prolonged IgE-mediated cutaneous anaphylaxis in vivo.

170 mong patients with hymenoptera venom-induced anaphylaxis in whom the diagnosis would most probably ha

171 Anaphylaxis incidence was 1.64% (5/305 patients) for HBA

172 Anaphylaxis incidence was determined for HBAT and previo

173 IgE-mediated anaphylaxis included the following: NMBA (35%), antibiot

174 In contrast, the development of intestinal anaphylaxis, including diarrhea, mast cell activation, a

175 The incidence of anaphylaxis increased over time, and several inciting tr

176 A previous episode of anaphylaxis increased the risk for anaphylaxis in SCIT (

177 She had a history of anaphylaxis induced by consuming cashew nuts.

178 Approximately 40% of food-related anaphylaxis induced by LTPs requires nonsteroidal anti-i

179 Anaphylaxis is a life-threatening condition for which we

180 Anaphylaxis is a life-threatening emergency of which rel

181 Anaphylaxis is a life-threatening hypersensitivity react

182 Anaphylaxis is a potentially life-threatening allergic r

183 Despite its rarity, anaphylaxis is a potentially life-threatening medical em

184 Anaphylaxis is a potentially life-threatening systemic a

185 Anaphylaxis is a rapidly developing, life-threatening, g

186 Anaphylaxis is a serious systemic allergic reaction with

187 Anaphylaxis is a severe allergic reaction that is rapid

188 Anaphylaxis is a severe systemic hypersensitivity reacti

189 First-line treatment for Hymenoptera sting anaphylaxis is intramuscular adrenaline.

190 naphylaxis, recognition of specific types of anaphylaxis is likely to become important for optimal pr

191 However, severe anaphylaxis is rare, and therefore the immunotherapy tab

192 Anaphylaxis is the most severe and frightening of the al

193 The role of basophils in anaphylaxis is unclear.

194 of IL-33 in patients with MC-dependent food anaphylaxis is unknown.

195 f endotypes for food and drug allergy or for anaphylaxis lag behind.

196 -dependent and NSAID-independent LTP-induced anaphylaxis (LTP-A).

197 7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal

198 gE, and the symptoms of passive IgE-mediated anaphylaxis, MC activation, Ca(2+) -mobilization and the

199 ing basophils was significantly lower during anaphylaxis (median, 3.5 cells/muL) than 7 and 30 days l

200 um markers) were significantly higher during anaphylaxis (median, 658 pg/mL) than in convalescent sam

201 llergic symptoms and protected all mice from anaphylaxis-mediated death after allergen challenge.

202 vere envenomation by arthropods or reptiles, anaphylaxis might even provide a survival advantage.

203 nts presented with Hymenoptera venom-induced anaphylaxis, no skin lesions, and baseline serum tryptas

204 Systemic anaphylaxis occurred in Was(-/-) mice (95%) with a morta

205 ylaxis, 2% non-IgE-mediated anaphylaxis, 12% anaphylaxis of unknown cause and 27% deemed non-anaphyla

206 ic IgE antibodies and manifestation of acute anaphylaxis on challenge.

207 ic IgE-mediated responses and drive systemic anaphylaxis on ingestion challenge.

208 sociated allergic reactions, including fatal anaphylaxis, on subsequent venom exposure.

209 There were no reports of anaphylaxis or reports consistent with severe laryngopha

210 ents, systemic allergic reactions (including anaphylaxis), or neutralising antibodies were reported.

211 h as acute asthma exacerbation, urticaria or anaphylaxis, or an exacerbation of allergic conjunctivit

212 ently identified as a suitable biomarker for anaphylaxis, outperformed ApoA1 with AUC=0.95.

213 Maternal OVA sensitization prevented food anaphylaxis, OVA-specific IgE production, and intestinal

214 with data generated using passive cutaneous anaphylaxis, ovalbumin-induced asthma and arthritis mode

215 Adrenaline use in hemodynamically stable anaphylaxis patient was independently associated with a

216 Adrenaline use in hemodynamically stable anaphylaxis patients was associated with a reduced risk

217 nt study we recruited 31 patients with acute anaphylaxis, predominantly to Hymenoptera venom.

218 tive cohort study of 761 adult patients with anaphylaxis presenting to the emergency department (ED)

219 Importantly, IgG-related anaphylaxis proceeds within a native context of activati

220 Mouse models of SCF-mediated anaphylaxis, radioprotection, and hematopoietic expansio

221 ctors activated per 1000 students at risk of anaphylaxis ranged from 6 to 8 per year, with consistent

222 echanisms involved in the different types of anaphylaxis, recognition of specific types of anaphylaxi

223 nd negative predictive value (NPV) of ST for anaphylaxis related to HBAT and other botulinum antitoxi

224 ound depletion of plasma S1P during systemic anaphylaxis rendered both platelet- and erythrocyte-deri

225 gnificant reduction in IgE sensitization and anaphylaxis reporting was seen.

226 s of PHO withdrawal on IgE sensitization and anaphylaxis reporting.

227 and the associated risk of life-threatening anaphylaxis requires vigilant management of peanuts in f

228 Statewide prevalence of anaphylaxis risk has increased in children attending Vic

229 0, 31.6), but did not overestimate non-fatal anaphylaxis risk or all-cause fatality risk.

230 nd salivary cortisol response to a simulated anaphylaxis scenario at 1 year.

231 Readouts included anaphylaxis scoring, quantification of allergen-specific

232 Specialist perioperative anaphylaxis services were surveyed through the Royal Col

233 and PHO were present at time of reaction and anaphylaxis severity grades were retrieved.

234 Anaphylaxis severity was evaluated based on hypothermia

235 dent mechanisms can act together to increase anaphylaxis severity.

236 life application to validate the new ICD-11 'Anaphylaxis' subsection.

237 to evaluate sensitivity and accuracy of the 'Anaphylaxis' subsection.

238 e cutaneous anaphylaxis and passive systemic anaphylaxis that can be used to investigate the pathogen

239 a-gal) are responsible for a delayed form of anaphylaxis that occurs 3-6 hours after red meat ingesti

240 specific IgG confers sensitivity to systemic anaphylaxis that relies on IgG Fc receptors (FcgammaRs).

241 ophenyl-BSA intravenously to induce systemic anaphylaxis that was monitored by using rectal temperatu

242 ology of allergic disorders, including fatal anaphylaxis, that it can be difficult to think of them i

243 Among 226 patients with suspected anaphylaxis, the diagnosis was confirmed in 124 (54.9%)

244 on, fluid extravasation, and the severity of anaphylaxis through a VE IL-4Ralpha/ABL1-dependent mecha

245 components were significantly protected from anaphylaxis to all 5 oral peanut challenges, as indicate

246 lowing all the relevant diagnostic terms for anaphylaxis to be included into the ICD-11 framework, WH

247 alternata) and OVA-induced models of active anaphylaxis to determine the DC-specific function of ADA

248 dine (PHO) is a postulated cause of allergic anaphylaxis to neuromuscular blocking agents (NMBAs).

249 ization to Pru p 3 in vivo, a mouse model of anaphylaxis to peach has been produced and changes in th

250 basophil activation in patients with delayed anaphylaxis to red meat providing further confirmation f

251 gitis related to cow's milk, and (3) delayed anaphylaxis to red meat.

252 tuximab (CTX) and is associated with delayed anaphylaxis to red meat.

253 Children presenting with anaphylaxis to the Montreal Children's Hospital were rec

254 rts (2005-2013) to the Norwegian Network for Anaphylaxis under Anaesthesia (NARA), total number of re

255 medicine in food allergy, drug allergy, and anaphylaxis under the auspices of the PRACTALL collabora

256 from food- to insect venom- and drug-induced anaphylaxis up to age 10 years, and there were few chang

257 lori-derived immunomodulators showed reduced anaphylaxis upon allergen sensitization and challenge, i

258 There is an increased risk of anaphylaxis upon peanut introduction in siblings of chil

259 We used a model of peanut allergy and anaphylaxis, various knockout mice, adoptive transfer ex

260 The estimated incidence rate of anaphylaxis was 26 cases per 100 000 person-years and th

261 The overall incidence rate of anaphylaxis was 42 per 100,000 person-years from 2001-20

262 Oral anaphylaxis was abrogated in Kit(W-sh/W-sh) mice and res

263 FCER1A expression during anaphylaxis was also significantly lower than in convale

264 Intestinal and systemic anaphylaxis was assessed, and the role of the high-affin

265 y STAT3 blockade, mast cell mediator-induced anaphylaxis was blunted in Stat3 mutant mice with AD-HIE

266 Anaphylaxis was defined as per World Allergy Organisatio

267 Anaphylaxis was evaluated in mice deficient for FcgammaR

268 Mammalian meat-induced delayed anaphylaxis was found in 8.6% of the participants with a

269 Passive systemic anaphylaxis was induced by injection of heat-aggregated

270 Anaphylaxis was inhibited by platelet-activating factor

271 Food-related anaphylaxis was most common in children aged 0 to 9 year

272 in children aged 0 to 9 years, venom-related anaphylaxis was most common in those 20 to 39 years of a

273 0 to 39 years of age, and medication-related anaphylaxis was most common in those 30 to 39 years of a

274 Anaphylaxis was significantly associated with a diagnosi

275 istamine- and IgE-mediated passive cutaneous anaphylaxis) we topically applied fingolimod prophylacti

276 In a model of systemic anaphylaxis, we found no difference between WT and Munc1

277 Six hundred thirty-one cases of anaphylaxis were identified.

278 In total 1053 hospital attendances for anaphylaxis were identified: 89 among non-Western immigr

279 The files clinically validated as being anaphylaxis were manually blind-coded under ICD-10 and c

280 analyze how quickly patients presenting with anaphylaxis were treated in emergency and whether treatm

281 ive and active oral antigen- and IgE-induced anaphylaxis were used to define the requirements of the

282 ically known as a slow reactive substance of anaphylaxis, were detected in PLY-treated lungs.

283 ergy and adverse reaction details, including anaphylaxis, were identified by using a student question

284 screening for this sensitivity as a cause of anaphylaxis, where reactions to alpha-gal are delayed an

285 ated and 91% of OIT-treated mice experienced anaphylaxis whereas only 21% of BF2+OIT-treated mice exh

286 Unexpectedly, K9.361 injection induced mild anaphylaxis, which was both FcgammaRIIB and FcgammaRIII

287 d FcgammaR-deficient mice were used to study anaphylaxis, which was induced by injection of 2.4G2 (ra

288 protects against allergen sensitization and anaphylaxis while reducing ILC2 induction.

289 Of the 340 patients with anaphylaxis who were normotensive at first presentation,

290 relationships of age group, sex, and year of anaphylaxis with incidence rates were assessed by fittin

291 We then compared patients after acute anaphylaxis with several control groups (nonallergic, hi

292 tment of mice with a history of food-induced anaphylaxis with the ABL kinase inhibitor imatinib prote

293 review is to recognize the presentations of anaphylaxis with the description of its current phenotyp

294 mAb induces and then suppresses IgG-mediated anaphylaxis without affecting IgE-mediated anaphylaxis.

295 , significantly reduced the severity of oral anaphylaxis without affecting the systemic TH2 response

296 phylaxis but prevented intact K9.361-induced anaphylaxis without diminishing intact K9.36 suppression

297 maRIII, and strongly suppressed IgG-mediated anaphylaxis without strongly affecting IgE-mediated anap

298 IgE antibody levels and protected mice from anaphylaxis, without affecting Th2 cells.

299 entification of pigeon ticks as a trigger of anaphylaxis would greatly improve medical care and advic

300 scents are at the highest risk of death from anaphylaxis, yet few population-based studies have descr