ライフサイエンスコーパス: oral tolerance

1 uestioned whether the thymus was involved in oral tolerance.

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

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

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

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

6 during the induction of oral priming versus oral tolerance.

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

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

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

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

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

12 portant for the induction and maintenance of oral tolerance.

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

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

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

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

17 really inserted corticosteroid implants; and oral tolerance.

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

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

20 the functional expression of iNOS regulates oral tolerance.

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

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

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

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

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

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

27 esults in systemic hyporesponsiveness termed oral tolerance.

28 immune responsiveness using mouse models of oral tolerance.

29 ucosal immune system in the establishment of oral tolerance.

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

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

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

33 ate of immunologic hyporesponsiveness termed oral tolerance.

34 immune nonresponsiveness in a process termed oral tolerance.

35 d their redundancy during the development of oral tolerance.

36 e associated with the development of natural oral tolerance.

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

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

39 crobiota play a critical role in maintaining oral tolerance.

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

41 treatments do not disrupt the development of oral tolerance.

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

43 ained in desensitizing allergic children via oral tolerance.

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

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

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

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

48 Pro-TH2 cytokines prevent oral tolerance.

49 es that interferes with the establishment of oral tolerance.

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Oral tolerance and inflammatory responses in the gut are

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 Oral tolerance cannot occur in murine models lacking T r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 Oral tolerance induced by DNFB gavage was impaired in ge

116 7.1 intact Ab or Fab fragments inhibited the oral tolerance induced by low-dose (0.5 mg) but not high

117 Oral tolerance induced with allogeneic cells shares char

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 Oral tolerance induction was enhanced in mice lacking ex

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

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

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

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

137 Ag administration are critical parameters in oral tolerance induction.

138 tion of antigen contributes significantly to oral tolerance induction.

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

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

141 Oral tolerance is a well-characterized phenomenon in ani

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

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

144 Oral tolerance is an immunomodulatory mechanism used by

145 However, oral tolerance is associated with decreased production o

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

147 Oral tolerance is mediated through active suppression by

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

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

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

151 Oral tolerance is the result of a complex immunoregulato

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 Oral tolerance prevents pathological inflammatory respon

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

168 Oral tolerance refers to the ability of the mucosal immu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Oral tolerance to food proteins is likely to be intimate

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

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

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

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

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

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

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

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

199 Oral tolerance to the Th2 allergic response was in large

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

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

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

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

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

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

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

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

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

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

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

211 Oral tolerance was successfully induced to OVA and peanu

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

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

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

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

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

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

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

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

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

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

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

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