ライフサイエンスコーパス: oral tolerance

1 of food allergy and the immune mechanisms of oral tolerance.

2 nursed by TLR2(-/-) dams exhibited impaired oral tolerance.

3 ained in desensitizing allergic children via oral tolerance.

4 ing in mature, balanced immune responses and oral tolerance.

5 In contrast, feeding of Ags alone leads to oral tolerance.

6 retinoic acid-dependent manner to allow for oral tolerance.

7 lerization; a phenomenon akin to gut-induced oral tolerance.

8 es that interferes with the establishment of oral tolerance.

9 uestioned whether the thymus was involved in oral tolerance.

10 regulatory T cells is a primary mechanism of oral tolerance.

11 ses to the gut flora in the establishment of oral tolerance.

12 pacity of an allergen to induce prophylactic oral tolerance.

13 han PPs in antigen sampling and induction of oral tolerance.

14 during the induction of oral priming versus oral tolerance.

15 d its receptor in the induction of high dose oral tolerance.

16 T cells is not influenced by the presence of oral tolerance.

17 mune functions, such as mucosal immunity and oral tolerance.

18 nd by the ability of Abs to MCP-1 to inhibit oral tolerance.

19 TS induced this blockade on the induction of oral tolerance.

20 portant for the induction and maintenance of oral tolerance.

21 P-1 deletional mice, indicating induction of oral tolerance.

22 ceptor CCR2 is required for the induction of oral tolerance.

23 cosal immunity may be a better way to assess oral tolerance.

24 lls and suggest that they may be involved in oral tolerance.

25 really inserted corticosteroid implants; and oral tolerance.

26 by donor transgenic T cells was critical for oral tolerance.

27 tudy was to examine the role of IFN-gamma in oral tolerance.

28 the functional expression of iNOS regulates oral tolerance.

29 le is critical for the induction of low-dose oral tolerance.

30 essential role in the induction of low-dose oral tolerance.

31 the primary cytokines that mediates low-dose oral tolerance.

32 egulation does not play an essential role in oral tolerance.

33 esults in systemic hyporesponsiveness termed oral tolerance.

34 immune responsiveness using mouse models of oral tolerance.

35 ucosal immune system in the establishment of oral tolerance.

36 ic protein (MCP)-1 as a regulatory factor of oral tolerance.

37 the gamma delta T cells altered induction of oral tolerance.

38 is critical to establishing and maintaining oral tolerance.

39 ate of immunologic hyporesponsiveness termed oral tolerance.

40 eins resulting from an impaired induction of oral tolerance.

41 a (RELMbeta)(3,4) is a critical regulator of oral tolerance.

42 cific pT(reg) cells and for establishment of oral tolerance.

43 that RORgammat-lineage APCs are required for oral tolerance.

44 ells (DCs) are required for anti-CD3-induced oral tolerance.

45 et in the case of spontaneous acquisition of oral tolerance.

46 t their presence underlies the phenomenon of oral tolerance.

47 Pro-TH2 cytokines prevent oral tolerance.

48 ic cells (DCs) in offspring was required for oral tolerance.

49 o play an important role in the induction of oral tolerance.

50 ere critical, for pT(reg) cell induction and oral tolerance.

51 leading to the failure to develop or loss of oral tolerance.

52 immune nonresponsiveness in a process termed oral tolerance.

53 d their redundancy during the development of oral tolerance.

54 e associated with the development of natural oral tolerance.

55 during which the microbiota imprints durable oral tolerance.

56 ulatory T cell (T(reg)) numbers and impaired oral tolerance.

57 ead to sensitization, but instead to partial oral tolerance.

58 crobiota play a critical role in maintaining oral tolerance.

59 ed regulatory T cells, anergy to cancer, and oral tolerance.

60 treatments do not disrupt the development of oral tolerance.

61 tives to determine the role of the thymus in oral tolerance: 1) as a site for the induction of regula

62 pensable role for GRAIL in T cell anergy and oral tolerance-a promising, antigen-specific strategy to

63 Although col(V)-induced oral tolerance abrogates rejection of minor histoincompa

64 nergy and/or deletion as the mechanism(s) of oral tolerance after high Ag doses.

65 (DC) have the responsibility of establishing oral tolerance against these Ags while initiating immune

66 s and the Peyer's patch (PP) in induction of oral tolerance and address the potential in vivo role of

67 role of breast-feeding in the development of oral tolerance and allergic diseases is controversial, w

68 ms have been identified for i.v. vs low dose oral tolerance and B cells are a predominant component o

69 s now established as a principal mediator of oral tolerance and can be recognized as the sine qua non

70 n these mechanisms might promote the loss of oral tolerance and development of food allergies.

71 t insights into the mechanisms that regulate oral tolerance and dietary antigen sampling have reveale

72 lled or sonicated allogeneic cells to induce oral tolerance and enhance corneal graft survival indica

73 such as those involved in the development of oral tolerance and food allergies.

74 hat plays a major role in the development of oral tolerance and host-defense mechanisms.

75 ing of the immune mechanisms responsible for oral tolerance and how perturbations in these mechanisms

76 ms and functional consequences of failure of oral tolerance and how these may be modulated to enhance

77 oral tolerance, explore the relation between oral tolerance and inflammatory bowel disease, and comme

78 Oral tolerance and inflammatory responses in the gut are

79 odulation, influencing epithelial integrity, oral tolerance and inflammatory responses.

80 as key regulators of immunity to pathogens, oral tolerance and intestinal inflammation.

81 t mediators in the intestine regulating both oral tolerance and mucosal inflammation.

82 protist Tritrichomonas (T.) arnold promotes oral tolerance and protects against reovirus- and murine

83 tagonism in the peri-weaning period restores oral tolerance and protects genetically prone offspring

84 ernal TLR2 affects the normal development of oral tolerance and related immune parameters during lact

85 s establish R-eTACs as critical mediators of oral tolerance and suggest novel cellular targets to mod

86 that MCP-1 is not required for induction of oral tolerance and that MCP-1 and CCR2 are essential for

87 es for the commensal microbiome in promoting oral tolerance and the association of intestinal dysbios

88 The exact mechanisms breaking oral tolerance and the effector pathways driving food al

89 d in the context of underlying mechanisms of oral tolerance and the establishment of gut colonization

90 cells are not necessary for the induction of oral tolerance, and allergic activation of mast cells do

91 xp3(+) regulatory T cell induction, impaired oral tolerance, and more severe colitis.

92 DCs) have been shown to play a major role in oral tolerance, and this function has been associated wi

93 This suppression (oral tolerance) appears to be due to the generation of m

94 med at early introduction of foods to induce oral tolerance are now being re-evaluated.

95 at the systemic immune mechanisms supporting oral tolerance are sufficient to promote long-term graft

96 Recently, clinical trials have used oral tolerance as a therapy for certain chronic inflamma

97 The attempt to induce oral tolerance as a treatment for food allergy has been

98 Such mucosally induced tolerance (oral tolerance) associated with induction of Ag-specific

99 tablished, would be an important property of oral tolerance, because it would allow treatment of auto

100 gh the skin can be prevented by induction of oral tolerance before skin exposure.

101 The development of oral tolerance begins in early life during a "window of

102 s, including IL-10, are believed to regulate oral tolerance, but direct evidence is lacking.

103 ceptor CCR2 is critical for the induction of oral tolerance by regulating Ag presentation leading to

104 meostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T ce

105 Together, we conclude that CD11b facilitates oral tolerance by suppressing Th17 immune differentiatio

106 ar-modified antigens might be used to induce oral tolerance by targeting SIGNR1 and LPDCs.

107 Oral tolerance cannot occur in murine models lacking T r

108 yp c 1 but not of mCyp c 1 induced long-term oral tolerance, characterized by lack of parvalbumin-spe

109 dietary antigens, classically referred to as oral tolerance, comprises a distinct complement of adapt

110 model of hyper-IgE and asthma, we found that oral tolerance could be effectively induced in the absen

111 B and rLTB, failed to block the induction of oral tolerance, demonstrating a stringent requirement fo

112 ructure-function relationship in PS-mediated oral tolerance, demonstrating that specific PS configura

113 fferent mechanisms are involved in mediating oral tolerance depending on the dose fed.

114 The roles of mast cells in oral tolerance development have not previously been exam

115 n, and histamine receptor 1 or 2 blockade on oral tolerance development in mice.

116 al route could be a valuable contribution to oral tolerance development in the decisive period of mic

117 mplications in (food) allergy prevention and oral tolerance development.

118 gulatory T cells, may reinforce induction of oral tolerance, even after the onset of arthritis.

119 outline the recent advances in understanding oral tolerance, explore the relation between oral tolera

120 It remains controversial whether oral tolerance extends to diminished mucosal IgA respons

121 In sum, these data support plant cell-based oral tolerance for suppression of inhibitor formation ag

122 We found that oral tolerance for Th1-type responses to OVA is maintain

123 mportant role for MCP-1 in the regulation or oral tolerance for the prevention and treatment of autoi

124 Oral tolerance has been argued to depend on "special" pr

125 s experimental autoimmune encephalomyelitis, oral tolerance has been used to protect against paralysi

126 Although the investigation of oral tolerance has classically involved Ag feeding, we h

127 , yet whether it contributes to induction of oral tolerance has not been documented.

128 nductive events leading to the generation of oral tolerance have not been well defined.

129 tigen-specific tolerance regimens, including oral tolerance, have been used prophylactically to preve

130 examine the conditions necessary to produce oral tolerance in a chronic relapsing model of EAE in B1

131 lamina propria (LPDCs) for the induction of oral tolerance in a model of food-induced anaphylaxis.

132 1, were analyzed for their ability to induce oral tolerance in a murine model.

133 The defective oral tolerance in CD11b(-/-) mice can be restored by ado

134 of other AMs and hastens the development of oral tolerance in children with IgE-mediated CMA.

135 onents that are essential for development of oral tolerance in early life and demonstrate the importa

136 experimental observations, the relevance of oral tolerance in human health has achieved new prominen

137 mall intestinal immune-mediated diseases and oral tolerance in humans.

138 ponses are responsible for the generation of oral tolerance in humans.

139 pTreg cell proliferation for re-establishing oral tolerance in immune-mediated food sensitivities.

140 fundamental difference in the mechanisms of oral tolerance in mice and humans requires a more focuse

141 sis of bystander suppression associated with oral tolerance in mice in vitro and in vivo.

142 Oral tolerance in microMT and wild-type mice was found t

143 results of studies of experimentally induced oral tolerance in patients with inflammatory bowel disea

144 nical data when available, the importance of oral tolerance in sustaining immunological nonresponsive

145 c variables that may affect the induction of oral tolerance in the gut and the mechanisms elucidated

146 athway is a potential strategy for enhancing oral tolerance in the setting of autoimmune and inflamma

147 nvestigate the benefit of APTs in predicting oral tolerance in these patients.

148 ss of p38alpha in DCs prevented induction of oral tolerance in vivo.

149 animal studies and with known mechanisms of oral tolerance in which lower doses of orally administer

150 Oral tolerance induced by DNFB gavage was impaired in ge

151 However, XCL1 was not required for oral tolerance induced by fed Ags, indicating that a dif

152 ly, oral administration of anti-CD3 enhanced oral tolerance induced by fed MOG(35-55) peptide, result

153 7.1 intact Ab or Fab fragments inhibited the oral tolerance induced by low-dose (0.5 mg) but not high

154 Oral tolerance induced with allogeneic cells shares char

155 To test the hypothesis that oral tolerance induces an immune deviation of T cells, p

156 The anti-MCP-1 abrogation of oral tolerance induction also resulted in restoration of

157 ares effectiveness and efficacy estimates of oral tolerance induction among different risk strata and

158 f RelB in DCs further results in an impaired oral tolerance induction and a marked type 2 immune bias

159 The mechanism of oral tolerance induction and maintenance is not well und

160 blockade of B7-H1/CD80 interaction prevented oral tolerance induction and restored T-cell responsiven

161 hat proinflammatory cytokines interfere with oral tolerance induction and that blocking the IL-6 path

162 -specific IgA antibody responses and lack of oral tolerance induction are all associated with aging.

163 eting protein Ag delivery system facilitates oral tolerance induction because of a reduction in Ag-sp

164 Also, MCP-1 has been reported to regulate oral tolerance induction by inhibition of Th1 cell-relat

165 Previous studies have suggested that oral tolerance induction by low doses of Ag is mediated

166 ly, MCP-1 upregulation was shown to regulate oral tolerance induction by the ability of antibodies to

167 controlled trials exploring the efficacy of oral tolerance induction in infancy for the prevention o

168 Successful oral tolerance induction is crucially dependent on micro

169 ed mast cell activation was initiated during oral tolerance induction or OVA immunization.

170 Oral tolerance induction through early introduction of a

171 disrupt gut immune homeostasis and prevents oral tolerance induction to bystander food antigen throu

172 nstrate cellular and molecular mechanisms of oral tolerance induction to food and aeroallergens in hu

173 Further studies that explore the efficacy of oral tolerance induction to other common food allergens

174 trolled trials investigating the efficacy of oral tolerance induction to peanut have enabled detailed

175 Oral tolerance induction was enhanced in mice lacking ex

176 or "Dupilumab" or "milk desensitization" or "oral tolerance induction" or "oral immunotherapy" or "Et

177 ersists, novel treatment options may include oral tolerance induction, although most authors do not c

178 To clarify the role of Peyer's patches in oral tolerance induction, BALB/c mice were treated in ut

179 nce of carp parvalbumin to digestion affects oral tolerance induction.

180 nfancy affects immune system development and oral tolerance induction.

181 y include immunization, viral infections and oral tolerance induction.

182 Ag administration are critical parameters in oral tolerance induction.

183 tion of antigen contributes significantly to oral tolerance induction.

184 tions at key checkpoints (CKPTs) that govern oral tolerance induction.

185 ion on hematopoietic cells was necessary for oral tolerance induction.

186 ing to assess whether PA can be prevented by oral tolerance induction.

187 in antigen (Ag) delivery system would induce oral tolerance instead of enhancement of Ag-specific muc

188 Oral tolerance is a well-characterized phenomenon in ani

189 Consistent with defective in vitro anergy, oral tolerance is abolished in vivo in OT-II TCR transge

190 genic systems suggests that the induction of oral tolerance is accompanied by priming of Ag-specific

191 Oral tolerance is an immunomodulatory mechanism used by

192 However, oral tolerance is associated with decreased production o

193 Oral tolerance is defined as the specific suppression of

194 lymph node, where Treg cells are induced and oral tolerance is established.

195 ot the exclusive mechanism by which low dose oral tolerance is induced.

196 Oral tolerance is mediated through active suppression by

197 feeding a neoantigen in an attempt to induce oral tolerance is not successful in patients with inflam

198 s study indicate that the inductive phase of oral tolerance is preceded by Ag-specific T cell activat

199 One of the proposed mechanisms of oral tolerance is the induction of Tregs.

200 Oral tolerance is the process by which feeding of solubl

201 Oral tolerance is the result of a complex immunoregulato

202 Oral tolerance is thought to have a central role in supp

203 ugh induction of T cell responses to fed Ag (oral tolerance) is thought to happen within the organize

204 bystander suppression has been described in oral tolerance, it is not known how its effects are medi

205 Loss of oral tolerance (LOT) to gluten, driven by dendritic cell

206 mucosal adjuvants to block the induction of oral tolerance may be a superior method for measuring mu

207 ed to treat early on in the disease process, oral tolerance may be considered to prevent disease prog

208 o food Ags, our current understanding of why oral tolerance may fail and sensitization may occur, and

209 nonimmunogenic through a poorly understood "oral tolerance" mechanism that involves immunosuppressiv

210 To induce oral tolerance, mice were fed with low-dose ovalbumin be

211 In an oral tolerance model, BTLA-deficient mice were found res

212 In a low-dose oral tolerance model, WT but not F4/80(-/-) mice generat

213 GFbeta1 and dimaprit increased the degree of oral tolerance obtained.

214 The bass' oral tolerance of gyrinidal varies broadly as a function

215 y to develop FA and an impaired induction of oral tolerance only in young males, which could be relat

216 e light has been thrown on the mechanisms of oral tolerance (or, more correctly, orally-induced syste

217 with dietary proteins for the development of oral tolerance, predisposing to the acquisition of food

218 V collagen (col(V)), and that col(V)-induced oral tolerance prevented acute and chronic rejection.

219 Oral tolerance prevents pathological inflammatory respon

220 vered within the intestinal tract to promote oral tolerance prior to weaning.

221 Oral tolerance promotes the suppression of immune respon

222 indings will motivate further exploration of oral-tolerance-promoting protists in CeD and other immun

223 is critical for inflammation regulation and oral tolerance promotion.

224 Finally, we used the antigens in an oral tolerance protocol to preventively protect mice fro

225 Limiting i.v. Ag dose or using an oral tolerance protocol yielded the greatest numbers of

226 Oral tolerance refers to the ability of the mucosal immu

227 tion of systemic tolerance to fed Ags (i.e., oral tolerance) rely on the steady-state migration of sm

228 ) cDCs impaired their polarization, although oral tolerance remained intact.

229 siderations in the successful application of oral tolerance strategies for suppression of chronic dis

230 l Ag because it has been used extensively in oral tolerance studies, and target cells expressing the

231 Oral tolerance tests for vitamin D2 (1,000 IU vitamin D2

232 her inhibitory cytokines in the induction of oral tolerance, TGF-beta 1 null mice and controls were g

233 vely regulates two of the main mechanisms of oral tolerance, TGF-beta production and clonal deletion

234 neous Ag (MBP) is more effective at inducing oral tolerance than heterogeneous Ag (myelin).

235 cteria, indicative of a broader breakdown of oral tolerance than hitherto appreciated.

236 rmine whether a single priming could prevent oral tolerance, the high-dose peanut regimen was applied

237 stand the human mucosal immune system before oral tolerance therapy for autoimmune and chronic inflam

238 select animal models, trials have begun for oral tolerance therapy for Crohn's disease.

239 and comment on the likelihood of successful oral tolerance therapy for inflammatory bowel disease.

240 incongruous that clinicians would try to use oral tolerance therapy to alleviate the symptoms of infl

241 ely thought to be caused by the breakdown of oral tolerance through a combination of genetic and envi

242 ating dietary antigen exposure and promoting oral tolerance, thus connecting decades of clinical obse

243 We further analyzed oral tolerance to a bystander food allergen, ovalbumin (

244 nhance corneal graft survival indicates that oral tolerance to alloantigens can occur via the indirec

245 ne (IL-4) were needed for the development of oral tolerance to alloantigens.

246 aft (WKY) lungs and abrogated col(V)-induced oral tolerance to allograft (F344) lungs.

247 Further evaluation of oral tolerance to CI in patients with SSc is justified t

248 f current studies of the basic mechanisms of oral tolerance to dietary antigen and of increasing reco

249 T cells (pTreg cells) play a central role in oral tolerance to dietary antigens and can contribute to

250 T(reg) cells, immunological homeostasis and oral tolerance to dietary antigens in the small intestin

251 emonstrate that TLR4 conditions induction of oral tolerance to DNFB through licensing tolerogenic gut

252 sed the question of whether Cop 1 can induce oral tolerance to EAE similar to myelin basic protein (M

253 anti-CD3 may serve as an adjuvant to enhance oral tolerance to fed Ags.

254 ained desensitization or even true long-term oral tolerance to food allergens through mechanisms that

255 adversely affecting the capacity to develop oral tolerance to food antigen in early life.

256 Oral tolerance to food proteins is likely to be intimate

257 sensitivity characterized by a breakdown of oral tolerance to gluten proteins in genetically predisp

258 proinflammatory cytokines, and induction of oral tolerance to gluten.

259 data indicates that atopics have heightened oral tolerance to haptens (chemical allergens).

260 h TLR4 ligands might be useful to potentiate oral tolerance to haptens and alleviate ACD in human sub

261 Induction of oral tolerance to haptens is an efficient way to prevent

262 hieve immunosuppression in the brain through oral tolerance to myelin basic protein (MBP).

263 environment in early life sets the stage for oral tolerance to new antigens in adult life.

264 mma delta TCR and inhibited the induction of oral tolerance to OVA, as measured by Ab, CD4+, and CD8+

265 Development of oral tolerance to ovalbumin, levels of tolerogenic CD103

266 Moreover, oral tolerance to oxazolone, mediated by Tregs, was impa

267 y about Peanut Allergy study, Persistance of Oral Tolerance to Peanut study, and Peanut Allergy Sensi

268 t organized Peyer's patches are required for oral tolerance to proteins, whereas haptens elicit syste

269 We examined whether oral tolerance to the contact sensitizer 2,4-dinitro-flu

270 Oral tolerance to the Th2 allergic response was in large

271 er initial excitement, clinical trials using oral tolerance to treat autoimmune disease have been som

272 on of Ag leads to systemic unresponsiveness (oral tolerance) to the fed Ag.

273 The results of an oral tolerance trial in Crohn's disease patients in Isra

274 tal autoimmune disease, a major mechanism of oral tolerance triggered by oral administration of antig

275 ith this, TCRdelta(-/-) mice did not develop oral tolerance upon oral administration of anti-CD3.

276 on the susceptibility of progeny to develop oral tolerance versus FA to cow's milk proteins (CMP) wa

277 Oral tolerance was assessed in 2 mast cell-deficient mur

278 The data also suggest that the impaired oral tolerance was at least partly caused by the absence

279 Oral tolerance was examined in BALB/c mice after the ado

280 Oral tolerance was impaired in CD69(-/-) and IFN-I recep

281 Moreover, oral tolerance was impaired in Rag2(R229Q) mice, and tra

282 Oral tolerance was induced by DNFB gavage in germ-free a

283 Oral tolerance was induced in mice fed high-dose peanut

284 trast to wild-type control animals, in which oral tolerance was induced, intragastric administration

285 Oral tolerance was investigated by feeding high-dose pea

286 Oral tolerance was successfully induced to OVA and peanu

287 administration, including the development of oral tolerance, was explored with the use of OVA TCR-tra

288 To examine the role of B cells in oral tolerance we fed low doses of OVA or myelin oligode

289 ght to be one mechanism for the promotion of oral tolerance, we attempted to induce tolerance in norm

290 hed murine model of allergic lung disease or oral tolerance, we evaluated the in vivo activity of Tre

291 e of cytokine regulation in the induction of oral tolerance, we fed OVA to mice deficient in Th1 (Sta

292 costimulatory molecules in the induction of oral tolerance, we have tested the effect of anti-B7.1 o

293 To address the role CCL2 plays in oral tolerance, we used both CCL2(-/-) and CCR2(-/-) mic

294 In contrast, sensitization and oral tolerance were not impaired in TSLPR(-/-) mice.

295 re are back-up mechanisms in place to induce oral tolerance when secretory IgA is lacking.

296 e (of at least 6 months) on the induction of oral tolerance when they are coadministered with the ant

297 However, only LysoPS successfully induced oral tolerance, whereas double-chain PS did not.

298 The ingestion of protein antigen can induce oral tolerance, which is mediated in part by a subset of

299 response to an ingested innocuous antigen is oral tolerance, which requires either gut DCs or a subse

300 orally induced peripheral immune tolerance (oral tolerance) without compromising APC maturation or a