ライフサイエンスコーパス: immune tolerance

1 urenine pathway which augments tumor-induced immune tolerance.

2 ectly to T cells, resulting in a bias toward immune tolerance.

3 ll immunity, whereas immature DCs can induce immune tolerance.

4 reducing osteoclast precursors and promoting immune tolerance.

5 ng miR-155 have an impaired ability to break immune tolerance.

6 3, and can suppress inflammation and promote immune tolerance.

7 which drives regulatory T-cell responses and immune tolerance.

8 of this regulatory DNA element in promoting immune tolerance.

9 esolution of organ damage and maintenance of immune tolerance.

10 e T-regulatory cells in tumor tissue promote immune tolerance.

11 ve processes to promote Treg homeostasis and immune tolerance.

12 age mouse blastocysts, which induces central immune tolerance.

13 is immune-mediated and adaptation represents immune tolerance.

14 umans, and it was accomplished by inhibiting immune tolerance.

15 diated DNA demethylation of Foxp3 to promote immune tolerance.

16 ing the oral mucosa to antigen may stimulate immune tolerance.

17 commensal microbiota and its contribution to immune tolerance.

18 nt a suitable approach to induce Ag-specific immune tolerance.

19 tolerance and ultimately in the breakdown of immune tolerance.

20 s being developed with the goal of restoring immune tolerance.

21 have potential as powerful tools to mediate immune tolerance.

22 through the PD-1/PD-L1 pathway is central to immune tolerance.

23 s through which ATRA may contribute to liver immune tolerance.

24 tion of environmental factors that influence immune tolerance.

25 are each independently required to maintain immune tolerance.

26 d Treg functions in CxLNs and disrupting CNS immune tolerance.

27 Treg heterogeneity in maintaining peripheral immune tolerance.

28 mmune system interactions and development of immune tolerance.

29 egulation, inflammatory signal pathways, and immune tolerance.

30 t and modulate host inflammation and promote immune tolerance.

31 y T cell and MDSC populations that augmented immune tolerance.

32 f the present understanding of fetus-induced immune tolerance.

33 elated with alloantigen-specific immunity or immune tolerance.

34 modulating the immune response and promoting immune tolerance.

35 direct targeting of immune cells to generate immune tolerance.

36 Autoimmune diseases result from a break in immune tolerance.

37 uces a semi-mature phenotype associated with immune tolerance.

38 fect on the inflammatory component of innate immune tolerance.

39 on and trafficking that orchestrates mucosal immune tolerance.

40 affect the inflammatory component of innate immune tolerance.

41 ) play a critical role in the maintenance of immune tolerance.

42 llergic disease and induce allergen-specific immune tolerance.

43 pitopes seen by bNAbs mimic self, leading to immune tolerance.

44 so plays a central role in pregnancy-induced immune tolerance.

45 ells represents a new approach for achieving immune tolerance.

46 portant for mucosal induction of Ag-specific immune tolerance.

47 its pDC and TLR to establish B cell-mediated immune tolerance.

48 ion phase and their ability to persist under immune tolerance.

49 ed on activated T cells for the induction of immune tolerance.

50 le to regulate adaptive immunity and promote immune tolerance.

51 for mature Treg identity and maintenance of immune tolerance.

52 fibrotic liver was tightly related to innate immune tolerance.

53 d function but is dispensable for peripheral immune tolerance.

54 s that regulate mucosal barrier function and immune tolerance.

55 n in vivo role for granzyme A in maintaining immune tolerance.

56 f T cell function contributing to peripheral immune tolerance.

57 cal modulators of both thymic and peripheral immune tolerance.

58 n of DC maturation is a central mechanism of immune tolerance.

59 ating DCs as key mediators of organ-specific immune tolerance.

60 vity of this enzyme has been associated with immune tolerance.

61 -10(+) regulatory T cells, which may promote immune tolerance.

62 atory T (Treg) cells, a lineage critical for immune tolerance.

63 been recognized as an important mechanism in immune tolerance.

64 an attractive way to induce antigen-specific immune tolerance.

65 NS) resulting from a breakdown in peripheral immune tolerance.

66 Tregs) are critical regulators of peripheral immune tolerance.

67 a process critical for establishing central immune tolerance.

68 regulated to balance immune activation with immune tolerance.

69 rgan graft survival and that they can induce immune tolerance, accelerate recovery from AKI, and prom

70 we examined whether the context of placental immune tolerance affected the functions of resident macr

71 The development and maintenance of immune tolerance after allogeneic hematopoietic stem cel

72 of antithymocyte globulin [ATG]) facilitates immune tolerance after bone marrow transplantation (BMT)

73 that increasing its expression might restore immune tolerance against allergens through the induction

74 godendrocyte glycoprotein-loaded DCs carried immune tolerance against the subsequent development of M

75 Immune tolerance and activation depend on precise contro

76 apoptosis via a FasL/Fas pathway results in immune tolerance and ameliorates the osteopenia phenotyp

77 ential of 1,25D3-mDCs to restore Ag-specific immune tolerance and arrest autoimmune disease progressi

78 tus, and expression of genes associated with immune tolerance and BCR signaling.

79 viral defense, with evidence for its role in immune tolerance and cancer cell behavior.

80 eplication but is implicated in establishing immune tolerance and chronic infection.

81 ullination have been linked to the breach of immune tolerance and clinical autoimmunity.

82 otypic anti-inflammatory cells that maintain immune tolerance and counteract tissue damage in a varie

83 r, which has a critical role in establishing immune tolerance and determining the fate of tumors.

84 ls (MDSCs) play a critical role in promoting immune tolerance and disease growth.

85 Prostaglandin E2 promotes not only immune tolerance and epithelial homeostasis but also the

86 is continuously required for maintenance of immune tolerance and for a major part of their character

87 s) play a pivotal role in the maintenance of immune tolerance and hold great promise as cell therapy

88 onal fitness of Treg cells in the control of immune tolerance and homeostasis.

89 uired to maintain the subtle balance between immune tolerance and immune response in the Drosophila g

90 neal layers contribute to immunogenicity and immune tolerance and into the key factors that limit vis

91 d at lower efficiency to sensitively control immune tolerance and memory cell population size, but th

92 Foxp3(+) regulatory T cells (Tregs) maintain immune tolerance and play an important role in immunolog

93 Epitope-optimization is required to break immune tolerance and potently activate AFP-specific CD8

94 ered to create an effective vaccine to break immune tolerance and potently activate CD8 T cells to pr

95 (Tregs) play a critical role in maintaining immune tolerance and preventing autoimmune disease.

96 pTregs, but not tTregs, mediates the loss of immune tolerance and promotes allograft rejection.

97 a single TACI mutation displayed a breached immune tolerance and secreted antinuclear antibodies (AN

98 hronic inactivation of pickle causes loss of immune tolerance and shortened lifespan.

99 110delta inhibitors can break tumour-induced immune tolerance and should be considered for wider use

100 ing, suggesting that PGI2 signaling promotes immune tolerance and that clinical use of COX-inhibiting

101 ally regulates the maintenance of peripheral immune tolerance and the functional maturation of pro-TG

102 The hormonal milieu influences immune tolerance and the immune response against viruses

103 mmune reconstitution and re-establishment of immune tolerance and their therapeutic potential followi

104 a novel molecular target in APCs to overcome immune tolerance and tips the balance toward T cell immu

105 ed in cancer and is thought to contribute to immune tolerance and tumor growth.

106 With our growing knowledge of immune tolerance and ways to overcome it, combination tr

107 f the immune system but also for maintaining immune tolerance, and more recent work has begun to iden

108 cell function and maintenance of peripheral immune tolerance, and mutations in its coding gene cause

109 ease in these cells implies the induction of immune tolerance, and the alanine aminotransferase (ALT)

110 role in the establishment and maintenance of immune tolerance, and this role is disrupted in diabetes

111 olecular mechanisms underlying tumor-induced immune tolerance are largely unknown.

112 However, the drivers of intratumoral immune tolerance are uncertain.

113 (LOS) after previous exposure to LOS induced immune tolerance, as evidenced by reduced TNF-alpha and

114 naturally formed nanoparticles expressed the immune tolerance-associated molecule 'programmed death-l

115 Infection and inflammation can disturb immune tolerance at the maternal-fetal interface, result

116 es of HIV-1 gp41 in man may be proscribed by immune tolerance because mice expressing the V(H) and V(

117 ce instead of having the normal TH1 bias and immune tolerance because of repeated exposure to pathoge

118 nism, which can contribute to maintenance of immune tolerance, becomes insufficient in allergic disea

119 Immune tolerance between the fetus and mother represents

120 ls not only contribute to the maintenance of immune tolerance, but also direct adverse immune reactio

121 esents a new type of immune cell involved in immune tolerance, but it also is a potential candidate f

122 as been known to play a role in induction of immune tolerance, but its role in the induction and main

123 LSECs are involved in induction of immune tolerance, but little is known about their functi

124 Dietary proteins usually induce immune tolerance, but may trigger life-threatening immun

125 bypasses many of the mechanisms involved in immune tolerance by allowing for expansion of tumor-spec

126 Induction of immune tolerance by an increase in regulatory T (Treg) c

127 f both sepsis lethality and the induction of immune tolerance by apoptotic cells.

128 er tyrosine kinase (Mer) signaling maintains immune tolerance by clearing apoptotic cells (ACs) and i

129 hat GARP exerts oncogenic effects, promoting immune tolerance by enriching and activating latent TGFb

130 Thus, Aire enforces immune tolerance by ensuring that distinct autoreactive

131 ein (CBL-B) is a key regulator of peripheral immune tolerance by limiting T cell activation and expan

132 Induction of immune tolerance by MAT-Fel d 1-ILIT involved multiple m

133 Thus, PPARgamma favors immune tolerance by promoting regulatory T cell generati

134 he delicate balance between inflammation and immune tolerance by skewing T-cell fate decisions toward

135 l repressor Capicua/CIC maintains peripheral immune tolerance by suppressing aberrant activation of a

136 COX inhibition abrogated immune tolerance by suppressing PGI2 IP signaling, sugge

137 We provide evidence that immune tolerance can be overcome in a murine model of ha

138 at cancer immunotherapy designed to overcome immune tolerance can be useful for a growing number of p

139 Immune tolerance caused by intrauterine contact with the

140 tumor inflammatory response, which increases immune tolerance, cell survival, and proliferation.

141 uction by Kupffer cells might promote innate immune tolerance, characterized by a lack of response to

142 Immune tolerance checkpoint inhibition has been transfor

143 st that BnAb development might be limited by immune tolerance controls.

144 Moreover, immune tolerance could be induced that precluded inducti

145 ent mechanisms involved in the regulation of immune tolerance could lead to new strategies to enhance

146 questions with regard to the role of DCs in immune tolerance could lead to the development of novel

147 nderstanding the link between metabolism and immune tolerance could lead to the identification of new

148 Maintenance of immune tolerance critically depends upon regulatory T ce

149 es, these three Ags exert major functions in immune tolerance, defense against infections, and antica

150 n this position paper, we review insights on immune tolerance derived from allergy and from cancer in

151 Methotrexate-induced immune tolerance does not seem to involve cell depletion

152 th food allergy who were not able to acquire immune tolerance during childhood.

153 Immune tolerance during human pregnancy is maintained by

154 of a state of operationally defined clinical immune tolerance during peanut OIT.

155 a novel, so far unknown role as modulator of immune tolerance during pregnancy.

156 nta, is a central component of fetus-induced immune tolerance during pregnancy.

157 ycin, to induce durable and antigen-specific immune tolerance, even in the presence of potent Toll-li

158 ditioning facilitates potent donor-recipient immune tolerance following bone marrow transplantation (

159 receptor (MC5r)-dependent pathway to recover immune tolerance following intraocular inflammation.

160 (Treg) are critical elements for maintaining immune tolerance, for instance to exogenous antigens tha

161 ious mechanisms that have been described for immune tolerance govern our ability to control self-reac

162 A growing understanding of immune tolerance has been the foundation for new approac

163 factor VIII as well as bypassing agents and immune tolerance have been reported as effective treatme

164 ivo at the start or stop of therapy impaired immune tolerance, highlighting the dependence of the the

165 ust be taken into account to demonstrate the immune tolerance hypothesis.

166 Cs can provide an effective means to restore immune tolerance in an already established autoimmune di

167 laboratory changes associated with clinical immune tolerance in antigen-induced T cells, basophils,

168 tion while concurrently restoring peripheral immune tolerance in autoimmune disease.

169 s were required for long-term maintenance of immune tolerance in both the CD4+ and CD8+ T cell compar

170 This suggests that the presumed immune tolerance in chronic HBV infections needs to be r

171 Apoptotic cells trigger immune tolerance in engulfing phagocytes.

172 mplete characterization of the mechanisms of immune tolerance in hematological malignancies is critic

173 0 dependent, as methotrexate does not induce immune tolerance in IL-10 knockout mice.

174 to the biotherapeutic can induce Ag-specific immune tolerance in mice through a mechanism that appear

175 d function in inhibiting aTreg-cell-mediated immune tolerance in mice.

176 mmune surveillance in MGUS and to break down immune tolerance in MM.

177 n should be considered as a basis to restore immune tolerance in MS.

178 are a subset of CD4(+) T cells that maintain immune tolerance in part by their ability to inhibit the

179 uman cartilage proteoglycan (PG) can promote immune tolerance in PG-induced arthritis (PGIA).

180 ovel findings have important implications on immune tolerance in pregnancy and beyond in areas of aut

181 lar aspects of immune dynamics: breakdown of immune tolerance in response to an infection with a path

182 r low-dose IL-2 therapy to enhance Tregs for immune tolerance in T1D.

183 inoid receptor 2 (CB2), in the regulation of immune tolerance in the gut and the pancreas.

184 P-treated autologous splenocytes resulted in immune tolerance in the host, including reduced dendriti

185 al period is a critical time for shaping the immune tolerance in the progeny, influencing development

186 ing the immune response to establish durable immune tolerance in type 1 diabetes remains a substantia

187 nt of iNKT-based therapies aiming to restore immune tolerance in type 1 diabetes.

188 ammatory potential and the ability to induce immune tolerance in vitro.

189 ainst CD3 called otelixizumab, which induces immune tolerance, in intestinal mucosa samples from pati

190 plays a crucial role in the establishment of immune tolerance, including both central tolerance and t

191 ce morbidity in patients before they undergo immune tolerance induction (ITI) and in those with persi

192 method to attempt to eliminate inhibitors is immune tolerance induction (ITI) via a protocol requirin

193 f tolerogenic therapies, other than standard immune tolerance induction (ITI), is an unmet goal.

194 The mechanism of immune tolerance induction appears to be IL-10 dependent

195 T in patients with such enzyme deficiencies, immune tolerance induction should be advocated in the pa

196 l ADA, we focused on identifying regimens of immune tolerance induction that may be readily available

197 titers > 1:80) in patients after successful immune tolerance induction therapy (n = 23), and 100% (n

198 of Th2-mediated inflammation, maintenance of immune tolerance, induction of the two suppressive cytok

199 herapy; thus, developing strategies to break immune tolerance is a high priority.

200 DC-mediated T cell immune tolerance is an active process that is influenced

201 ciphering cellular and molecular pathways of immune tolerance is an important goal, with the expectat

202 ls targeting hybrid peptides may explain how immune tolerance is broken in T1D.

203 more efficient methods to induce Ag-specific immune tolerance is critical to advancing allergy treatm

204 Immune tolerance is critical to the avoidance of unwarra

205 Immune tolerance is defined as nonresponsiveness of the

206 Immune tolerance is executed partly by Foxp3(+)regulator

207 These data may explain how peripheral immune tolerance is impaired in tissues under autoimmune

208 ource of antigenic peptides to which central immune tolerance is lacking.

209 for tissue-restricted self antigens, or how immune tolerance is maintained for self-antigen-specific

210 How immune tolerance is maintained in the skin remains uncle

211 Immune tolerance is necessary to prevent the immune syst

212 omote allergic airway diseases by inhibiting immune tolerance is not known.

213 contribution to either immune activation or immune tolerance is still not entirely understood.

214 reactive cells are silenced by mechanisms of immune tolerance, islet antigen-reactive B lymphocytes a

215 indicate that GPR15 plays a role in mucosal immune tolerance largely by regulating the influx of Tre

216 e a mechanism by which loss of AIRE-mediated immune tolerance leads to intestinal disorders in patien

217 This study is the first to show that immune tolerance may be impaired in spaceflight, leading

218 rus (AAV) gene therapy, exploiting a natural immune tolerance mechanism induced by human leukocyte an

219 This approach has allowed immune tolerance mechanisms limiting bnAb production to

220 iduals with autoimmune disease and defective immune tolerance mechanisms may produce BnAbs more readi

221 nization initiates CD4bs-bnAb responses, but immune tolerance mechanisms restrict their development,

222 Discovery of immune tolerance mechanisms, which inhibit pre-existing

223 Ns) are integral sites for the generation of immune tolerance, migration of CD4(+) T cells, and induc

224 response, the National Institutes of Health Immune Tolerance Network and JDRF established a multicen

225 liver transplant recipients enrolled in the Immune Tolerance Network immunosuppression withdrawal (I

226 tion approach with the potential to overcome immune tolerance observed in pregnancy, and lower vaccin

227 ngeneic bile duct antigens efficiently break immune tolerance of recipient mice, capturing several ke

228 Induction of immune tolerance pathways and reduction in egg allergy i

229 s B virus exploits these naturally occurring immune tolerance pathways to establish persistent postna

230 n Treg cells can be titrated to break tumour immune tolerance preferentially.

231 e aerosolized with ovalbumin (OVA) to induce immune tolerance prior to immune sensitization with an i

232 re), a transcription coordinator involved in immune tolerance processes, is a critical spindle-associ

233 y complex (MHC) class I molecule involved in immune tolerance processes, playing an important role in

234 asopharyngeal cells in vivo and show that an immune tolerance profile, characterized by elevated TGF-

235 tion-induced cell death (AICD) essential for immune tolerance regulation.

236 opment of therapeutic interventions in other immune tolerance-related diseases.

237 The mechanisms contributing to clinical immune tolerance remain incompletely understood.

238 the identity of such cells and their role in immune tolerance remains unclear.

239 Immune tolerance requires regulatory T (Treg) cells to p

240 Maintaining immune tolerance requires the production of Foxp3-expres

241 -/-) and PD-1(-/-) mice, which have impaired immune tolerance, resulted in a slightly greater injury.

242 n the context of the clinical translation of immune tolerance strategies, we discuss the significant

243 s demonstrate that in addition to peripheral immune tolerance, T cell-expressed FURIN is also a centr

244 rt-term costimulation blockade led to robust immune tolerance that could be transferred independently

245 une system immaturity by inducing a state of immune tolerance that facilitates HBV persistence.

246 Dendritic cells (DCs) can induce peripheral immune tolerance that prevents autoimmune responses.

247 However, the breakdown in immune tolerance that results in the induction and persi

248 autoimmune regulator (AIRE, which regulates immune tolerance) that allow self-reactive T cells to en

249 that APCs have a crucial role in maintaining immune tolerance, the underlying mechanisms are poorly u

250 F6 in directing DC maintenance of intestinal immune tolerance through balanced induction of Treg vers

251 esponse to inflammatory stimuli and promotes immune tolerance through effector T-cell anergy and enha

252 ) may be particularly favorable for breaking immune tolerance through PD-1 blockade.

253 oenvironment of established tumours promotes immune tolerance through poorly understood mechanisms.

254 ignificant impact on subsequent immunity and immune tolerance, thus placing them in a unique position

255 T (Treg) cells play a key role in sustaining immune tolerance to allergens, yet mechanisms by which T

256 a new interventional approach to restore the immune tolerance to allergens.

257 Immune tolerance to alpha-Gal in blood type B individual

258 Immune tolerance to avoid chronic immunosuppression is a

259 Finally, we suggest a unified model in which immune tolerance to beta cells can be broken by several

260 Immune tolerance to both self-antigens and innocuous non

261 pecific T cell response because of a lack of immune tolerance to C-terminal epitopes as a consequence

262 Although the spleen is a major site where immune tolerance to circulating innocuous antigens occur

263 S) mainly in young adults, and a breakage of immune tolerance to CNS self-antigens has been suggested

264 we sought to determine whether induction of immune tolerance to col(V) might ameliorate atherosclero

265 Mucosal inoculation successfully induced immune tolerance to col(V) with an accompanying reductio

266 on and anti-T-cell antibodies safely induces immune tolerance to combined hematopoietic cell and orga

267 neonatal life was required for establishing immune tolerance to commensal microbes.

268 ry T cells (Tregs) are required to establish immune tolerance to commensal microbes.

269 d with immunomodulatory reagents that target immune tolerance to established cancers.

270 V) vector-mediated gene therapy that induced immune tolerance to factor IX (FIX) in a hemophilia B (H

271 mmunotherapy, might lead to a restoration of immune tolerance to foods.

272 ng immunotherapeutic approaches to establish immune tolerance to foods.

273 Induction of immune tolerance to FVIII in hemophilia has been extensi

274 responses and promoting durable, functional immune tolerance to FVIII in patients with an existing i

275 Induction of specific immune tolerance to grafts remains the sought-after stan

276 that maternal microchimerism induces stable immune tolerance to non-inherited maternal antigens in o

277 autoimmune disease characterized by loss of immune tolerance to nuclear and cell surface antigens.

278 ompromise those mechanisms normally assuring immune tolerance to nuclear autoantigens.

279 Inducing immune tolerance to prevent rejection is a key step towa

280 Regulatory T cells (Tregs) mediate immune tolerance to self and depend on IL-2 for homeosta

281 immunity against pathogens while maintaining immune tolerance to self-Ags.

282 oimmune disease that results from a break in immune tolerance to self-antigens, leading to multi-orga

283 overcoming multiple mechanisms that mediate immune tolerance to self-antigens.

284 n has been associated with a break in innate immune tolerance to self-DNA.

285 P3 play a pivotal role in the maintenance of immune tolerance to self.

286 ignant hematologic disorders and can mediate immune tolerance to subsequent organ transplantation.

287 y known therapy that provides long-term host immune tolerance to the allergen, but is time-consuming

288 At this age, neonates acquire immune tolerance to the conditionally responsive lucifer

289 In contrast, END showed strong evidence for immune tolerance to the parasite, with high levels of ci

290 th the discovery of disease-specific loss of immune tolerance to the pyruvate dehydrogenase complex a

291 The immune tolerance was confirmed by marked reduction in ai

292 Immune tolerance was confirmed in all dogs after challen

293 Pregnancy induces a state of immune tolerance, which can result in spontaneous improv

294 tal adenocarcinoma (PDA) is characterized by immune tolerance, which enables disease to progress unab

295 high-affinity antigen receptors can overcome immune tolerance, which has been a major limitation of i

296 s in perpetuating the loss of liver-specific immune tolerance will be discussed.

297 In this review, we describe principles of immune tolerance with a focus on its breakdown during pa

298 The induction of immune tolerance with HSCs has led to isolation of other

299 robiome in the maintenance and disruption of immune tolerance with parallels in human studies.

300 e liver appears to be privileged in terms of immune tolerance, with a low incidence of antibody-media