ライフサイエンスコーパス: allergen-specific

1 Allergen-specific Ab responses were subsequently boosted

2 in infants at high risk of peanut allergy is allergen specific and does not prevent the development o

3 No relevant change in allergen-specific and total IgE levels was observed in s

4 ns from extracts of incurred chocolate using allergen-specific antibodies and human allergic sera.

5 Almost all allergen-specific antibodies were mutated, and binding t

6 Allergen-specific antibodies were produced in rabbits us

7 ion against allergen exposure in part due to allergen-specific antibodies.

8 rlying allergy comprises two components, the allergen-specific antibody (i.e. IgE, IgG) and the T-cel

9 Here, we investigated the association of allergen-specific antibody and T- as well as B-cell resp

10 296), the current study investigated the cat allergen-specific antibody responses.

11 The dissociation of allergen-specific antibody, and B- and T-cell responses

12 polyclonal IgG with CD64-IgE Fc established allergen-specific artificial sera that showed comparable

13 characterize the IgE sequences expressed by allergen-specific B cells and track the fate of these B-

14 vides the first detailed characterization of allergen-specific B cells before and after bee venom tol

15 epitope specificity, and clonal diversity of allergen-specific B cells in patients with food allergy

16 trol donors have a population of circulating allergen-specific B cells with the phenotype and functio

17 n with CFSE staining allow the dissection of allergen-specific B- and T-cell responses.

18 rtoires identified additional members of the allergen-specific B-cell clones.

19 We sought to characterize peanut allergen-specific B-cell populations and the sequences a

20 We hypothesized that PNOIT induces a clonal, allergen-specific B-cell response that could serve as a

21 cific (anti-IgE), helminth-specific, and HDM-allergen-specific basophil histamine release (HR), plus

22 We conducted a 7-year study of monitoring allergen-specific basophil response and serological mark

23 therapy induces sustained suppression of the allergen-specific basophil response that persists after

24 and TGF-beta, the production of IgG4 isotype allergen-specific blocking antibodies, and decreased all

25 The induction of allergen-specific blocking IgG antibodies represents an

26 According to immunogenicity and induction of allergen-specific blocking IgG antibodies, 4 hypoallerge

27 Here, we compared the induction of allergen-specific blocking IgG in outbred guinea pigs wh

28 enterotoxins promote TH2 differentiation of allergen-specific CD4 conventional T (Tcon) cells and as

29 model of airway inflammation, we found that allergen-specific CD4 T cells survived longer than 70 da

30 formed multimodal immunomonitoring to assess allergen-specific CD4 T-cell properties in parallel with

31 for the studying of cross-reactivity at the allergen-specific CD4(+) T cell level among DR04:01 rest

32 llergy interaction more fully, parasite- and allergen-specific CD4(+) T cell responses in 12 subjects

33 considered as optimal tools to characterize allergen-specific CD4(+) T cells, but this technique is

34 ed with clinical benefit than alterations of allergen-specific CD4(+) T-cell or IgG responses.

35 found that successful immunotherapy induces allergen-specific CD4+ T cells to expand and shift towar

36 Five of 57 allergen-specific cells belonged to clones containing Ig

37 Participants receiving placebo showed no allergen-specific changes.

38 The allergen-specific clones had increased persistence, high

39 These results broaden our understanding of allergen-specific desensitization and may provide a mech

40 assessed to identify cross-reactivity among allergen-specific DR04:01-restricted T-cells in six subj

41 Skewing of allergen-specific effector T and effector B cells to a r

42 These results demonstrate that allergen-specific gut inflammation in human PBMC-engraft

43 data provide a basis from which to evaluate allergen-specific human antibody repertoires in healthy

44 Support for the in vivo existence of allergen-specific human Breg cells comes from direct det

45 Allergen-specific human IgE in mouse sera, which was det

46 addition, blockade of IL-9 or IL-4 enhanced allergen-specific IFN-gamma production.

47 No association between the level of allergen-specific Ig responses and B- or T-cell prolifer

48 Levels of total serum IgE and allergen specific IgE antibodies towards 14 common inhal

49 crude allergen from jellyfish and evaluated allergen specific IgE antibody levels using ELISA.

50 es showed higher levels of jellyfish-derived allergen specific IgE than healthy control samples.

51 kness, cutaneous inflammation, and total and allergen specific IgE) following cutaneous allergen rech

52 xpansion of TH 2 cells and the production of allergen specific IgE.

53 ions and, eczema, sensitization (>/= 1 of 10 allergen-specific IgE >/= 0.35 IU/mL) and total IgE at a

54 years, and sensitization ever was defined as allergen-specific IgE >/=0.35 kUA /l to common food and/

55 hese samples, 48 patients with no detectable allergen-specific IgE (group A) and 44 patients with str

56 rotective effect for atopy defined as raised allergen-specific IgE (OR 0.75; 95% CI 0.62 - 0.92; P <

57 tially exacerbated and detected as increased allergen-specific IgE (sIgE) and IgG4 (sIgG4) levels and

58 mination at age 2 years to assess eczema and allergen-specific IgE (sIgE) and perform skin prick test

59 Serum total and allergen-specific IgE (sIgE) levels were measured by usi

60 gen specificity, 20% to 40% of children with allergen-specific IgE (sIgE) of 0.35 kU/L or greater had

61 This fusion protein allowed the induction of allergen-specific IgE Ab responses without allergen-spec

62 complexes were formed with human monoclonal allergen-specific IgE and Bet v 1.

63 Allergen-specific IgE and IgG antibody responses were de

64 The variability in allergen-specific IgE and IgG frequencies depends on exp

65 -MAPS) to the simultaneous detection of food allergen-specific IgE and IgG4 , and compared it with Im

66 h recombinant allergens, and measurements of allergen-specific IgE and IgG4 antibodies were performed

67 There were no significant differences in allergen-specific IgE and IgG4 levels, cytokine producti

68 cat allergen-specific T-cell frequency, cat allergen-specific IgE and IgG4 titers, and clinical stat

69 Allergen-specific IgE and IgG4 were detected in parallel

70 ponsiveness, respiratory symptoms, total and allergen-specific IgE and IgG4, immune function, and inf

71 tor TH1, TH2, and TH17 cells; suppression of allergen-specific IgE and induction of IgG4; and suppres

72 They are associated with allergen-specific IgE and nonallergic mechanisms that ma

73 Methylation biomarkers outperformed allergen-specific IgE and skin prick tests for predictin

74 Allergen-specific IgE antibodies are a hallmark of type

75 generation of allergen-specific T cells and allergen-specific IgE antibodies.

76 efit of ImmunoCAP is the obtained quantified allergen-specific IgE antibody level and the lack of int

77 Of 52 distinct allergen-specific IgE heavy chains from 8 allergic donor

78 tected in 68.0% and represented the only HBV allergen-specific IgE in 5% of the patients.

79 izumab or placebo on the levels of total and allergen-specific IgE in patients with birch pollen alle

80 g with blood eosinophil counts and total and allergen-specific IgE in sera, were also evaluated.

81 mented the short half-life of both total and allergen-specific IgE in serum.

82 Allergen-specific IgE is the causative agent of allergic

83 : eczema, skin prick tests (SPTs), increased allergen-specific IgE level (>/= 0.35 IU/mL), and doctor

84 the past 12 months, and at least 1 positive allergen-specific IgE level.

85 Allergen-specific IgE levels against seven common allerg

86 ells of allergic patients is correlated with allergen-specific IgE levels and determines allergen upt

87 For control purposes, total, allergen-specific IgE levels and omalizumab-IgE complexe

88 Overall 48.8% of the population had allergen-specific IgE levels of 0.3 ISAC standardized un

89 was based on history, skin test results, and allergen-specific IgE levels to HBV.

90 Smaller skin test results and lower allergen-specific IgE levels were predictive of successf

91 uantiBRITE beads and compared with total and allergen-specific IgE levels, as well as with allergen-i

92 in-Mreg before allergen challenge suppressed allergen-specific IgE levels, the influx of eosinophils

93 administration of allergen induced rises of allergen-specific IgE levels, whereas intranasal adminis

94 ian's diagnosis and symptoms but no positive allergen-specific IgE levels.

95 omalizumab did not enhance systemic total or allergen-specific IgE levels.

96 7 serum mediators, total IgE levels, and 130 allergen-specific IgE levels.

97 Allergen-specific IgE measurements and the clinical hist

98 partly explain why atopic subjects who make allergen-specific IgE never develop clinical symptoms, a

99 allergic effector cells permanently display allergen-specific IgE on their surface and immediately r

100 Repeated allergen encounter boosts allergen-specific IgE production and enhances clinical s

101 Our data thus indicate that allergen-specific IgE production is boosted by allergen

102 These cells could provide precursors for allergen-specific IgE production upon allergen re-exposu

103 oncomitant with the onset of lung pathology, allergen-specific IgE production, eosinophilia, and Th2

104 ity, bronchiolar inflammatory infiltrate and allergen-specific IgE production.

105 ongest predictive factor for the presence of allergen-specific IgE responses detected by ImmunoCAP wa

106 IT over two weeks could sufficiently inhibit allergen-specific IgE responses in mice suffering OVA-in

107 Thus, the presence of allergen-specific IgE responses may be re-assessed by Im

108 Examination of allergen-specific IgE revealed plasma IgE from DOCK8-def

109 (CRD) has become an accepted tool to detect allergen-specific IgE sensitization towards hundreds of

110 In the full model including all allergen-specific IgE subtypes as predictors, there were

111 The diagnostic accuracy of the recombinant allergen-specific IgE test could help to improve the sel

112 utine diagnosis of baker's allergy, however, allergen-specific IgE tests with whole wheat and rye flo

113 a cells (PCs) provide a continuous source of allergen-specific IgE that is central to allergic respon

114 n prick test (SPT) and by the measurement of allergen-specific IgE to dust mites and cockroach in pla

115 Binding of allergen-specific IgE to its high-affinity receptor Fcep

116 tibody gene sequencing and identification of allergen-specific IgE with combinatorial antibody fragme

117 CD4 and CD8 T cells, eosinophils, total IgE, allergen-specific IgE, and urinary cotinine were measure

118 d to the number of FcepsilonRI occupied with allergen-specific IgE, as well as the dose and valency o

119 of MSC action, immunologic assays including allergen-specific IgE, cellular IL-10 production, and al

120 Total and allergen-specific IgE, IgG and basophil sensitivity were

121 Concentrations of allergen-specific IgE, IgG1, IgG4 and IgA to seven Bet v

122 aternal 25(OH)D concentrations and offspring allergen-specific IgE, total IgE, and eosinophil cationi

123 lergen application induces rises of systemic allergen-specific IgE, we performed a double-blind place

124 vitro Th2 responses precede the detection of allergen-specific IgE, which can provide a window of opp

125 tigated the IgE recognition of Phl p 1 using allergen-specific IgE-derived single-chain variable Ab f

126 177 IU/mL, P = .002), and nonfungal inhalant allergen-specific IgE.

127 desensitization in mice: down-regulation of allergen-specific IgE.

128 vation, and TH2 cytokine responses and serum allergen-specific IgE/IgG1 levels.

129 by intradermal testing or serum testing for allergen-specific IgE; crude extracts are the basis for

130 Allergen-specific IgEs clustered into 7 groups that migh

131 ot the sole contributor to the clustering of allergen-specific IgEs.

132 nts had positive test responses to 1 or more allergen-specific IgEs.

133 aeroallergen-specific IgE and corresponding allergen-specific IgG (sIgG) and associated immunophenot

134 upon immunization of animals induced higher allergen-specific IgG Abs than the wild-type allergens a

135 in combination with LT from E. coli induced allergen-specific IgG antibodies blocking allergic patie

136 These findings suggest that allergen-specific IgG antibodies can act to induce and s

137 On immunization, they induced allergen-specific IgG antibodies, which inhibited patien

138 body level and the lack of interference from allergen-specific IgG antibodies.

139 Animal models have demonstrated that allergen-specific IgG confers sensitivity to systemic an

140 Our previous studies demonstrated that allergen-specific IgG immune complexes (ICs) and house d

141 DM allergens than nonasthmatic children, but allergen-specific IgG levels were comparable.

142 Allergen-specific IgG was administered to mice undergoin

143 tion with rDer p 2 induced similar levels of allergen-specific IgG1 and IgE antibodies in both mouse

144 lted in augmented Th2 immunity and increased allergen-specific IgG1 and IgE.

145 s by adaptive immune mechanisms that involve allergen-specific IgG1 antibodies and plasma or regulato

146 ivity as well as a simultaneous detection of allergen-specific IgG4 , as a potential parameter for to

147 It is recommended to explore the use of allergen-specific IgG4 as a biomarker for compliance.

148 Although allergen-specific IgG4 can block IgE-mediated allergen p

149 Detectable allergen-specific IgG4 could be determined only for low

150 n reactivity was significantly decreased and allergen-specific IgG4 responses were significantly elev

151 IgE response were associated with increased allergen-specific IgG4 synthesis early in therapy.

152 unotherapy can stimulate somatic mutation of allergen-specific IgG4.

153 roup, P = .03) and a significant increase in allergen-specific IgG4.

154 Allergen-specific IgGs are known to inhibit IgE-mediated

155 l levels restores their capacity to activate allergen-specific IL-10-Tregs .

156 ' DCs with increased levels of GILZ generate allergen-specific IL-10-Tregs again.

157 pared the ability of patients' DCs to induce allergen-specific IL-10-Tregs before and after an in viv

158 cording to clinical data, the restoration of allergen-specific IL-10-Tregs is required to control res

159 h SCIT alone led to a sustained reduction in allergen-specific IL-4-producing cell counts (P < .01).

160 molecular compounds from pollen enhance the allergen specific immune response in the skin and nose.

161 e clinical desensitization and modulation of allergen-specific immune parameters including augmented

162 ted with characteristic modifications in the allergen-specific immune response, but a detailed synthe

163 t of basophil sensitivity and an increase in allergen-specific immunoglobulin concentration.

164 The poor correlation between allergen-specific immunoglobulin E (asIgE) and clinical

165 trate the detection of low concentrations of allergen-specific Immunoglobulin E (IgE) in human sera u

166 he EN ISO 15189 standard was carried out for allergen-specific immunoglobulin E determination using t

167 deterioration in asthma symptoms, change in allergen-specific immunoglobulin G4 (IgG4), change in as

168 Serum was analyzed for allergen-specific immunoglobulin levels.

169 Measurements of allergen-specific immunoglobulins are not suitable for d

170 Allergen specific immunotherapy has been shown to be the

171 icable, and easy to manufacture vaccines for allergen-specific immunotherapy (AIT) has been limited b

172 Allergen-specific immunotherapy (AIT) has been used for

173 Allergen-specific immunotherapy (AIT) induces specific b

174 Allergen-specific immunotherapy (AIT) is the only availa

175 While allergen-specific immunotherapy (AIT) is very efficient

176 It is still unclear whether allergen-specific immunotherapy (AIT) with birch pollen

177 PIT) is proposed as an alternative route for allergen-specific immunotherapy (AIT).

178 Allergen-specific immunotherapy (ASIT) is used to treat

179 ggest for the use as adjuvant and carrier in allergen-specific immunotherapy (ASIT).

180 Recently, epicutaneous allergen-specific immunotherapy (EPIT) has proven effect

181 Epicutaneous allergen-specific immunotherapy (EPIT) is proposed as an

182 e results of our third trial on epicutaneous allergen-specific immunotherapy (EPIT) will be presented

183 Human studies demonstrated that allergen-specific immunotherapy (IT) represents an effec

184 cell response of vitamin D as an adjunct to allergen-specific immunotherapy (IT).

185 Allergen-specific immunotherapy (SIT) faces problems rel

186 tion with LT may be a promising strategy for allergen-specific immunotherapy against birch pollen all

187 lergic reactions are common in the course of allergen-specific immunotherapy and even occur with alle

188 he development of a vaccine for grass pollen allergen-specific immunotherapy based on two recombinant

189 However, subcutaneous allergen-specific immunotherapy can also induce anaphyla

190 ess has been made through the development of allergen-specific immunotherapy encompassing 3 major for

191 common food hypersensitivities worldwide but allergen-specific immunotherapy for shellfish allergy is

192 Subcutaneous allergen-specific immunotherapy is a standard route for

193 Efficacy of allergen-specific immunotherapy is often severely impair

194 The goal of allergen-specific immunotherapy is the induction of prot

195 Allergen-specific immunotherapy is the only curative tre

196 Allergen-specific immunotherapy is the only known therap

197 h as probiotics have not proved helpful, but allergen-specific immunotherapy may be disease modifying

198 ought to evaluate the efficacy and safety of allergen-specific immunotherapy using 2 dose regimens of

199 Allergen-specific immunotherapy was associated with pref

200 Allergen-specific immunotherapy with SHAS-OVA as compare

201 ction of their increase during the course of allergen-specific immunotherapy, as well as their increa

202 an be used to monitor the blocking effect of allergen-specific immunotherapy-induced non-IgE antibodi

203 lergic patients during the build-up phase of allergen-specific immunotherapy.

204 ncer, hepatitis, and malaria vaccines and in allergen-specific immunotherapy.

205 rategy to improve the efficacy and safety of allergen-specific immunotherapy.

206 pe I sensitization and determine its role in allergen-specific immunotherapy.

207 vidual allergen-derived epitopes change over allergen-specific immunotherapy.

208 lergen binding is one important mechanism of allergen-specific immunotherapy.

209 tudied were anaphylaxis management plans and allergen-specific immunotherapy.

210 epresent promising vaccines for birch pollen allergen-specific immunotherapy.

211 fusion proteins can enhance the efficacy of allergen-specific immunotherapy.

212 This shows that allergen-specific in vitro Th2 responses precede the det

213 Instead, lifelong reactivity is conferred by allergen-specific long-lived memory B cells that repleni

214 specific IgE, cellular IL-10 production, and allergen-specific lymphocyte proliferation were performe

215 in the peripheral blood and stool mucus and allergen-specific lymphocyte stimulation test.

216 ponses to subsequent allergen exposure in an allergen-specific manner, effectively preventing or reve

217 the"LOW"responders, four cases showed >/=10% allergen-specific maximum histamine release.

218 tent allergen exposure, we hypothesized that allergen- specific memory Th2 cells are present and the

219 nced the capacity of CD1c(+) DCs to activate allergen-specific memory CD4(+) T cells.

220 xposure on the generation and persistence of allergen-specific memory T cells in asthmatic patients a

221 Altogether, we believe that allergen-specific memory T cells reside and function in

222 llergic sensitization, but whether these are allergen specific or increase susceptibility to poly-sen

223 omplex latent structure involving 7 age- and allergen-specific patterns in the COPSAC2000 birth cohor

224 ctivation of inflammasome, and generation of allergen-specific peripheral T-cell tolerance.

225 In addition, Treg cells reduced allergen-specific proliferation and cytokine production

226 or Alternaria, and the effect of inhibiting allergen-specific protease activities on IL-33 levels wa

227 h the proportion of serum total IgE that was allergen-specific (r = 0.615, P < 0.05).

228 allergen tolerance include the induction of allergen-specific regulatory subsets of T and B cells, t

229 es (IgG-IC) via breast milk and induction of allergen-specific regulatory T (T reg) cells in offsprin

230 Allergen-specific regulatory T and Breg cells orchestrat

231 panding populations of naturally suppressive allergen-specific regulatory T cells (Tregs).

232 ogical mechanisms underlying the boosting of allergen-specific secondary IgE Ab responses and the all

233 Our results indicate that allergen-specific secondary IgE Ab responses can be boos

234 hich had been used for sensitization boosted allergen-specific secondary IgE responses without a dete

235 nsus regions, except in early life, although allergen-specific sensitization differs based on sociode

236 hin a racially diverse birth cohort using 10 allergen-specific serum IgE (sIgE) measurements from chi

237 om more than 6500 children were analyzed for allergen-specific serum IgE against common allergens.

238 luded anaphylaxis scoring, quantification of allergen-specific serum IgE and IgG1 and of the mast cel

239 ion status and related phenotypes [total and allergen-specific serum IgE, bronchial hyperresponsivene

240 gn and assess an accreditation procedure for allergen-specific serum IgE.

241 ar irrespective of the allergen specificity, allergen-specific serum immunoglobulin E concentration,

242 Allergen-specific serum immunoglobulin E concentrations

243 Allergen-specific serum immunoglobulin E detection and q

244 Allergen-specific serum immunoglobulin E determination w

245 surements including positive SPT or elevated allergen-specific serum/plasma IgE levels.

246 sitive skin prick testing (SPT), or elevated allergen-specific serum/plasma immunoglobulin (Ig) E lev

247 phoproliferation experiments, they contained allergen-specific T cell epitopes required for tolerance

248 epitope-derived peptide of Phl p 1 devoid of allergen-specific T cell epitopes, as recognized by BALB

249 oosted by repetitive B cell epitopes without allergen-specific T cell help by cross-linking of the B

250 f allergen-specific IgE Ab responses without allergen-specific T cell help.

251 secondary IgE responses without a detectable allergen-specific T cell response.

252 lymphocytes and results in the generation of allergen-specific T cells and allergen-specific IgE anti

253 SEA promoted TH2 responses of allergen-specific T cells and asthma pathogenesis by act

254 Allergen-specific T cells can be identified by HLA class

255 Transcriptomic analysis of allergen-specific T cells defined genes modulated in con

256 IgE complexes into B cells and activation of allergen-specific T cells depended on IgE binding to CD2

257 mportant role in controlling the activity of allergen-specific T cells through IgE-facilitated allerg

258 on by reducing the priming and activation of allergen-specific T cells, as well as the production of

259 characterize different TH functionalities of allergen-specific T cells, ELISPOT assays with sets of o

260 unt of inhaled allergen is low, by expanding allergen-specific T cells.

261 to the draining lymph nodes, and priming of allergen-specific T cells.

262 r of antigens demonstrated to be targeted by allergen-specific T cells.

263 sed to identify novel antigens recognized by allergen-specific T cells.

264 C population, consistent with recruitment of allergen-specific T cells.

265 PS animals also accumulated large numbers of allergen-specific T regulatory (Treg) cells with high le

266 AT-Fel d 1 group, characterized by increased allergen-specific T regulatory cells, decreased circulat

267 body responses were determined by ELISA, and allergen-specific T- and B-cell responses were measured

268 Allergen uptake and allergen-specific T-cell activation in relation to CD23

269 gE levels and influences allergen uptake and allergen-specific T-cell activation.

270 ecific gating allowed discriminating between allergen-specific T-cell and B-cell responses.

271 ght to evaluate the relationship between cat allergen-specific T-cell frequency, cat allergen-specifi

272 s has been observed, cross-reactivity at the allergen-specific T-cell level has been less documented.

273 Data on early allergen-specific T-cell responses in allergic children

274 We sought to characterize allergen-specific T-cell responses linked with allergy o

275 ort of peanut-allergic participants, we used allergen-specific T-cell sorting and single-cell gene ex

276 The marked increase in APC function for allergen-specific TC proliferation during allergic infla

277 ) ) cells expressed more CD200R than the non-allergen-specific Th2 (CD154(-) CRTh2(+) ) cells.

278 e, both PLA2denat -MB formulations decreased allergen-specific Th2 CD4 T-cell reactivity.

279 Preferential allergen-specific TH2 cell deletion after repeated high-

280 was associated with preferential deletion of allergen-specific TH2 cells and without a significant ch

281 To avert the differentiation of allergen-specific Th2 cells in atopic individuals is a m

282 potential of a functional assay quantifying allergen-specific Th2 cells in CMA children.

283 Allergen-specific TH2 cells most closely paralleled the

284 Little is known about allergen-specific Th2 memory cells and their contributio

285 ligands IL-4 and IL-13 in the development of allergen-specific TH2 responses during the onset and chr

286 ver, mechanisms regulating acute and chronic allergen-specific TH2 responses in vivo remain incomplet

287 rmore, the development of disease as well as allergen-specific Th2 responses occurs despite deficienc

288 We hypothesized that allergen-specific Th2-cell responses can be detected pre

289 Allergic sensitization is initiated by allergen-specific Th2-cell responses.

290 that DEP exposure results in accumulation of allergen-specific TH2/TH17 cells in the lungs, potentiat

291 Beside avoidance, there is currently no allergen-specific therapy available.

292 of Immunity, Pepper and colleagues find that allergen-specific tissue-resident memory T cells are mai

293 er accounting for the ratio of component- or allergen-specific to total IgE can improve this predicti

294 chanisms that are suggested to contribute to allergen-specific tolerance.

295 need to be included in diagnostic tests and allergen-specific treatments in addition to group 1 alle

296 ributes to the allergic response by reducing allergen-specific Treg cell and activating mast cell cou

297 33-stimulated ILC2s blocks the generation of allergen-specific Treg cells and favors food allergy.

298 ke phenotype, also found in peripheral-blood allergen-specific Treg cells of food-allergic children.

299 impaired generation and function of mucosal allergen-specific Treg cells.

300 By expanding allergen-specific Tregs and reducing pro-inflammatory ef