ライフサイエンスコーパス: peripheral tolerance

1 dicating a non-redundant role in maintaining peripheral tolerance.

2 ptors may be generally important in systemic peripheral tolerance.

3 iately scaled immune responses and mediating peripheral tolerance.

4 s evidence that dendritic cells (DCs) induce peripheral tolerance.

5 t immune responses and playing a key role in peripheral tolerance.

6 s that regulate T cell response and maintain peripheral tolerance.

7 ole in maintenance of immune homeostasis and peripheral tolerance.

8 tic organs, suggesting a role in maintaining peripheral tolerance.

9 n optimal host defense against infection and peripheral tolerance.

10 t thereby play a central role in maintaining peripheral tolerance.

11 well as in the induction and maintenance of peripheral tolerance.

12 ells in the lymph nodes, suggesting impaired peripheral tolerance.

13 Rather, they are suppressed by mechanisms of peripheral tolerance.

14 B cell responses and plays a crucial role in peripheral tolerance.

15 mph node (LN) stroma in mediating CD8 T cell peripheral tolerance.

16 sthma and autoimmunity and shown to modulate peripheral tolerance.

17 angeable factors that influence the route to peripheral tolerance.

18 ve regulation of T-lymphocyte activation and peripheral tolerance.

19 play an important role in the maintenance of peripheral tolerance.

20 diabetes (T1D) relies on active induction of peripheral tolerance.

21 s to breach central, but not late, stages of peripheral tolerance.

22 implicating a breakdown of both central and peripheral tolerance.

23 d can suppress immune responses and maintain peripheral tolerance.

24 PCs, thus contributing to the maintenance of peripheral tolerance.

25 r chamber of the burned eye failed to induce peripheral tolerance.

26 cells are instrumental to the maintenance of peripheral tolerance.

27 cal role in regulating T cell activation and peripheral tolerance.

28 successful strategy to promote experimental peripheral tolerance.

29 disease and is regulated by both central and peripheral tolerance.

30 control the de novo generation of aTregs and peripheral tolerance.

31 is an important means for the maintenance of peripheral tolerance.

32 t self-antigens by mature lymphocytes, i.e., peripheral tolerance.

33 caused by a breakdown in central rather than peripheral tolerance.

34 of the B7 family, play an important role in peripheral tolerance.

35 responses, but may result in a breakdown in peripheral tolerance.

36 non-self pathogens can lead to breakdown of peripheral tolerance.

37 r steady-state maintenance of quiescence and peripheral tolerance.

38 targeted long-standing immune protection and peripheral tolerance.

39 d plays a critical role in the regulation of peripheral tolerance.

40 which this locus contributes to the loss of peripheral tolerance.

41 e eye and notes the parallels to gut-induced peripheral tolerance.

42 lls (Tregs) are important for maintenance of peripheral tolerance.

43 opulation of lymphocytes that contributes to peripheral tolerance.

44 that regulates lymphocyte proliferation and peripheral tolerance.

45 portant role for LAG-3 in adenosine-mediated peripheral tolerance.

46 play a critical role in maintaining dominant peripheral tolerance.

47 gs) play an important role in the control of peripheral tolerance.

48 nd hence is essential for the maintenance of peripheral tolerance.

49 h 1 ligand (PD-L) pathway is instrumental in peripheral tolerance.

50 negative regulation of immune responses and peripheral tolerance.

51 what extent this might be due to defects in peripheral tolerance.

52 rs their ability to maintain tissue-specific peripheral tolerance.

53 important contributions of both central and peripheral tolerance.

54 s (Tregs) play a pivotal role in maintaining peripheral tolerance.

55 itiating immune responses and in maintaining peripheral tolerance.

56 implicating TRAF6 as a critical mediator of peripheral tolerance.

57 r than deleting them, thus failing to induce peripheral tolerance.

58 a chain, is essential for the maintenance of peripheral tolerance.

59 in TCR signaling to enforce both central and peripheral tolerance.

60 utoimmune disorders and to the expression of peripheral tolerance.

61 egulate T cell activation and play a role in peripheral tolerance.

62 s play a critical role in the maintenance of peripheral tolerance.

63 pproach for the induction and maintenance of peripheral tolerance.

64 +Foxp3+ regulatory T (T(Reg))-cell-dependent peripheral tolerance.

65 ls (Treg) are thought to be important in the peripheral tolerance.

66 egulate T(H)1 responses and the induction of peripheral tolerance.

67 e pivotal for T cell survival, mobility, and peripheral tolerance.

68 onse to antigen, it may function to maintain peripheral tolerance.

69 t CD8+ T regulatory cells during eye-induced peripheral tolerance.

70 for DCs in the onset of innate immunity and peripheral tolerance.

71 cells that are pivotal in the regulation of peripheral tolerance.

72 curtailing effector T cells and establishing peripheral tolerance.

73 ipates in the control of inflammation and in peripheral tolerance.

74 re shown to be pivotal in the maintenance of peripheral tolerance.

75 shment of immune memory, and preservation of peripheral tolerance.

76 unity results from a breakdown in central or peripheral tolerance.

77 ls is thought to be important in maintaining peripheral tolerance.

78 gulatory T (Treg) cells play a major role in peripheral tolerance.

79 n microRNA (miRNA) regulation of central and peripheral tolerance.

80 biomaterials or mimicry of antigen-specific peripheral tolerance.

81 nditions, demonstrating the robust nature of peripheral tolerance.

82 e the central element for the maintenance of peripheral tolerance.

83 , is critical for immune cell activation and peripheral tolerance.

84 (PD-L1) and PD-L2 is crucial for maintaining peripheral tolerance.

85 nsistent with abortive T cell activation and peripheral tolerance.

86 play an important role in the maintenance of peripheral tolerance.

87 y, as well as the development of central and peripheral tolerance.

88 ionally inactivates CD4(+) T cells to induce peripheral tolerance.

89 c autoimmunity, but play a redundant role in peripheral tolerance.

90 peutic immune modulation is the induction of peripheral tolerance, a large part of which is mediated

91 associated immune deviation (ACAID) model of peripheral tolerance, a.c. inoculation of antigen into F

92 ctive NKT cells (required for development of peripheral tolerance) actually produced urokinase-type p

93 s an important mechanism in the induction of peripheral tolerance against autoimmune diseases, yet no

94 ortant roles of T(reg) in the maintenance of peripheral tolerance against self-Ag as well as the incr

95 These in vivo data indicate that peripheral tolerance alone can protect NOD8.3 mice from

96 m skin to draining lymph nodes (LN) to drive peripheral tolerance and adaptive immunity.

97 ion of KIRs in T cells profoundly influences peripheral tolerance and antigen-specific immune respons

98 (Treg) play an important role in maintaining peripheral tolerance and are potent suppressors of T-cel

99 hat FcgammaRIIB is an important regulator of peripheral tolerance and attenuation of the inhibitory s

100 mune diseases, how exactly it contributes to peripheral tolerance and autoimmunity is unclear.

101 lls (Tregs) are essential for maintenance of peripheral tolerance and can prevent and alleviate IBD.

102 isease resulting from defects in central and peripheral tolerance and characterized by T cell-mediate

103 egs) play a major role in the maintenance of peripheral tolerance and control of autoimmunity.

104 underlying the contribution of cytokines to peripheral tolerance and control of autoimmunity.

105 mportant homeostatic mechanism that supports peripheral tolerance and could be a target for the preve

106 im of providing an integrated view of T cell peripheral tolerance and fate regulation.

107 ated and has implications for maintenance of peripheral tolerance and for the development of autoimmu

108 rovides opportunities to study mechanisms of peripheral tolerance and generate antigen-specific regul

109 cells are fundamental to the maintenance of peripheral tolerance and have great therapeutic potentia

110 having a central role in the maintenance of peripheral tolerance and in shaping the repertoire of em

111 an effective therapeutic approach to restore peripheral tolerance and induce remission of AIH.

112 ceptor with an essential role in maintaining peripheral tolerance and is among the most promising imm

113 Nrp1 is essential for proper maintenance of peripheral tolerance and its absence can result in unche

114 Vsir (-/-) mice developed loss of peripheral tolerance and multi-organ chronic inflammator

115 T cell self-tolerance is thought to involve peripheral tolerance and negative selection, involving a

116 of inhibitory receptors is able to maintain peripheral tolerance and prevent autoimmunity.

117 itical role in the immune system to regulate peripheral tolerance and prevent autoimmunity.

118 T (Treg) cells are essential for maintaining peripheral tolerance and preventing autoimmunity.

119 rtance of MCs in conditioning DCs to mediate peripheral tolerance and shows a functional impact of pe

120 The ability of the tol-APC to induce peripheral tolerance and suppress existing Th2 immune in

121 cells also play critical role in maintaining peripheral tolerance and suppressing the development or

122 ate a crucial role of sGARP in modulation of peripheral tolerance and T effector cell function, openi

123 that some are involved in the maintenance of peripheral tolerance and the control or even help to res

124 tic susceptibility, resulting in the loss of peripheral tolerance and the development of cGVHD.

125 physiologic) IL-4/IL-13 in the regulation of peripheral tolerance and the development of T1D has yet

126 environmental IL-4/IL-13 and the HR play in peripheral tolerance and the development of T1D.

127 naling threshold, contribute to breakdown of peripheral tolerance and the entry of autoreactive B cel

128 orders offer novel insights into pathways of peripheral tolerance and their disruption in autoimmunit

129 the differential role of DRAK2 in central vs peripheral tolerance and to assess its impact on the dev

130 ific T-cell responses linked with allergy or peripheral tolerance and to determine how CD4(+) T-cell

131 used to understand mechanisms of central and peripheral tolerance and to evaluate more specific treat

132 4 and IL-13 contribute to the maintenance of peripheral tolerance and whether their function is coord

133 l-associated antigen passages contributes to peripheral tolerance, and antigen delivered by paracellu

134 lls (Tregs) are essential for maintenance of peripheral tolerance, and defects in Treg function have

135 immune responses and for the maintenance of peripheral tolerance, and have been extensively studied.

136 ognized role for TRAF6 in the maintenance of peripheral tolerance, and suggest the presence of a T ce

137 Tregs are essential for maintaining peripheral tolerance, and thus targeting these cells may

138 role of TRAF6 in an additional mechanism of peripheral tolerance, anergy.

139 However, peripheral tolerance appears maintained by selection thr

140 ls (Tregs) responsible for the generation of peripheral tolerance are under the tight regulation of t

141 tral deletion and regulatory T cell-mediated peripheral tolerance both play major roles in establishi

142 bioavailability of type I IFN contributes to peripheral tolerance breakdown through the activation of

143 contributors in induction and maintenance of peripheral tolerance, but a regulatory role has been als

144 to play a critical immunoregulatory role in peripheral tolerance, but its role in alloimmune respons

145 nd cytokine signaling in T cells to maintain peripheral tolerance, but the extent to which PTPN2 defi

146 ntribute significantly to the maintenance of peripheral tolerance, but they ultimately fail in autoim

147 conversion might provide a means to generate peripheral tolerance by "converting" potentially damagin

148 y-state lymphatic drainage may contribute to peripheral tolerance by delivering self-Ags to lymph nod

149 Lymphatic endothelial cells (LECs) induce peripheral tolerance by direct presentation to CD8 T cel

150 ression within the Treg compartment enhances peripheral tolerance by diverting these suppressive cell

151 y a crucial role in inducing and maintaining peripheral tolerance by driving the differentiation of A

152 -presenting cells exposed to TGF-beta induce peripheral tolerance by increasing IkappaB alpha express

153 Thus, PD-1-PD-L1 interactions maintain peripheral tolerance by mechanisms fundamentally distinc

154 ls, prevent autoimmune diseases and maintain peripheral tolerance by suppressing self-reactive effect

155 cyte-associated antigen 4 (CTLA-4) maintains peripheral tolerance by suppressing T-cell activation an

156 city and play essential roles in maintaining peripheral tolerance by suppressing the activation of se

157 onal tolerance, but also in the induction of peripheral tolerance by vascularized renal allografts in

158 In a model of peripheral tolerance called anterior chamber-associated

159 Peripheral tolerance can be achieved in many but not all

160 egulate onset of sEAE, and that induction of peripheral tolerance can be exploited to prevent/treat s

161 Various mechanisms of peripheral tolerance can protect against autoimmunity, i

162 These findings illuminate a peripheral tolerance checkpoint that aborts T-cell clona

163 ) may involve in part the impairment of this peripheral tolerance checkpoint.

164 Central and peripheral tolerance checkpoints are in place to remove

165 ta indicate that Sle1 perturbs the action of peripheral tolerance checkpoints operative on antinuclea

166 ators and networks that control the six main peripheral tolerance checkpoints throughout the life of

167 the bone marrow but inappropriately survive peripheral tolerance checkpoints, leading to the accumul

168 tibodies arise through defects in central or peripheral tolerance checkpoints.

169 pecific CD8(+) T cells, escaping central and peripheral tolerance, contribute to beta-cell destructio

170 In this study, we demonstrate a peripheral tolerance defect in the dendritic cells of NO

171 duced transient immune responses seen during peripheral tolerance development.

172 Also, we were able to induce peripheral tolerance directly in IL-13-deficient, IL-4/I

173 We propose that peripheral tolerance for internal organs relies on the c

174 for inhibitory molecules PD-L1 and PD-L2 in peripheral tolerance has been proposed.

175 Central and peripheral tolerance hinder the contribution of high-avi

176 the underlying mechanisms causing defective peripheral tolerance in ADA-SCID.

177 atory enzyme that supports Treg function and peripheral tolerance in adult life.

178 To examine peripheral tolerance in anti-insulin B cells, we generat

179 d dendritic cells has been shown to regulate peripheral tolerance in both murine and human studies.

180 cells, their relevance to the maintenance of peripheral tolerance in humans remains elusive.

181 al administration of soluble peptide induces peripheral tolerance in myelin basic protein (MBP)-speci

182 recognizing tau epitopes escape central and peripheral tolerance in relatively high numbers, and the

183 y T cell responses to pathogens and inducing peripheral tolerance in self-reactive T cells.

184 ressive immune responsiveness and generating peripheral tolerance in stringent allograft models are u

185 ification that may contribute to the loss of peripheral tolerance in T1D.

186 e function and that these cells also escaped peripheral tolerance in the presence of LYN-deficient de

187 50% reduction in natural Treg thymic output, peripheral tolerance in Traf6DeltaTEC mice was normal, w

188 ns and may have a role in the maintenance of peripheral tolerance in vivo.

189 Mechanisms involved in the induction of peripheral tolerance include T cell-intrinsic pathways,

190 cess might provide insights into central and peripheral tolerance induced by other professional and n

191 These results suggest that peripheral tolerance induced through the eye requires Ag

192 hat CD4(+)CD25(+) regulatory T cells mediate peripheral tolerance induced with mouse Tg in CBA mice.

193 The prevailing model for the induction of peripheral tolerance involves cross-presentation of tiss

194 ken together, these results demonstrate that peripheral tolerance is enhanced or diminished through m

195 Peripheral tolerance is essential for immunological home

196 ial of CD8(+) T cells, maintenance of CD8(+) peripheral tolerance is extremely important.

197 g) and, despite low overall Treg expression, peripheral tolerance is maintained.

198 Together these studies imply that peripheral tolerance is more complex than previously tho

199 Peripheral tolerance is partially controlled by the expr

200 Central and peripheral tolerance is required to prevent immune respo

201 expression of autoimmunity where a breach in peripheral tolerance is suspected.

202 dence that LECs are important in maintaining peripheral tolerance, limiting and resolving effector T

203 Thus, FcgammaRIIB can contribute to peripheral tolerance maintenance by inhibiting DC activa

204 s with myasthenia gravis, although disrupted peripheral tolerance may play a greater role in autoimmu

205 A major peripheral tolerance mechanism is the induction of anerg

206 res include central or thymic tolerance, and peripheral tolerance mechanisms acting after naive T cel

207 egulation in NINJA mice bypasses central and peripheral tolerance mechanisms and allows for robust en

208 toreactive may be important in understanding peripheral tolerance mechanisms and may provide insight

209 ) escape from thymic negative selection, and peripheral tolerance mechanisms are essential for their

210 Peripheral tolerance mechanisms are in place to prevent

211 Peripheral tolerance mechanisms exist to prevent autoimm

212 e mediated through disruption of central and peripheral tolerance mechanisms initiated by early cessa

213 ction tools to study in detail the ways that peripheral tolerance mechanisms limit the expansion and

214 We suggest that whereas thymic and peripheral tolerance mechanisms remove cells that can be

215 Both central and peripheral tolerance mechanisms selectively impinge on t

216 As such, our data indicate the existence of peripheral tolerance mechanisms that regulate the freque

217 udy the relative contribution of central and peripheral tolerance mechanisms to deletion of antigen-s

218 ually, these T cells are kept at bay through peripheral tolerance mechanisms, including regulation th

219 from a polyclonal repertoire by central and peripheral tolerance mechanisms.

220 y to be low avidity and nonresponsive due to peripheral tolerance mechanisms.

221 their FVIII-reactive lymphocytes relies upon peripheral tolerance mechanisms.

222 Fas ligand (FasL) is known to play a role in peripheral tolerance mediated by clonal deletion of Ag-s

223 Day 3 thymectomy (D3Tx) results in a loss of peripheral tolerance mediated by natural regulatory T ce

224 Moreover, induction of peripheral tolerance might act in part by affecting T ce

225 y adoptive transfer of F4/80(+) APCs in both peripheral tolerance models, indicating a central role f

226 srupting essential mechanisms of central and peripheral tolerance, more common human autoimmune disea

227 induction of clone 4 T cell apoptosis during peripheral tolerance occurred via an intrinsic death pat

228 tested the hypothesis that acute GVHD blocks peripheral tolerance of autoreactive T cells by impairin

229 important role for BTLA in the induction of peripheral tolerance of both CD4(+) and CD8(+) T cells i

230 overcome limitations imposed by central and peripheral tolerance on TCR affinity.

231 In this study, we investigated the effect of peripheral tolerance on the endogenous T(CD8) response t

232 cause uPA knockout (KO) mice did not develop peripheral tolerance or develop CD8(+) T regulatory cell

233 significant aberrations in their central and peripheral tolerance or in T lymphocyte activation.

234 Peripheral tolerance orchestrated by regulatory T cells,

235 e cytokines, such as IL-10, is essential for peripheral tolerance, particularly in the intestines.

236 These data demonstrate that breaching peripheral tolerance permits a cross-reactive HIV-1 auto

237 ient mice (lacking invariant NKT) to develop peripheral tolerance postintracameral inoculation of Ag.

238 Central and peripheral tolerance prevent autoimmunity by deleting th

239 Peripheral tolerance produced by ACAID requires the part

240 with disease, the most common seem to affect peripheral tolerance rather than central tolerance.

241 ibutions of iT reg cells and nT reg cells in peripheral tolerance remain unclear as a result of an in

242 cell functional unresponsiveness, in natural peripheral tolerance remains unclear.

243 re B cell stage, and a relaxed selection for peripheral tolerance, resulting in an increased frequenc

244 n type 1 diabetes, the breach of central and peripheral tolerance results in autoreactive T cells tha

245 ave a specialized role in the maintenance of peripheral tolerance, specifically, to generate suppress

246 urs in the presence of preserved central and peripheral tolerance, suggesting that diminished T-cell

247 y, in TCR-mediated AICD with implications in peripheral tolerance, T-cell homeostasis and cancer.

248 ant roles in regulating humoral immunity and peripheral tolerance than in effector T cell immunity.

249 The peripheral tolerance that arises after injection of anti

250 The peripheral tolerance that is elicited by the anterior ch

251 ciated immune deviation (ACAID) is a form of peripheral tolerance that is induced by introducing Ags

252 pe 1 diabetes may result from a breakdown in peripheral tolerance that is partially controlled by the

253 effector differentiation, defining a step in peripheral tolerance that provides insights into the phe

254 hus, i.v. inoculation of the tol-APC induced peripheral tolerance that suppressed Th2-mediated pathog

255 ngs, we suggest, necessitate a broadening of peripheral tolerance theory to include steady-state pres

256 ve B cells lacking Rasgrp1 break central and peripheral tolerance through both T cell-independent and

257 These data suggest that p27kip1 promotes peripheral tolerance through its ability to inhibit CDK2

258 T regulatory (Treg) cells enforce peripheral tolerance through regulation of diverse immun

259 ing impaired immune regulation and restoring peripheral tolerance through T-reg infusion in this cond

260 (DCs) play an important role in maintaining peripheral tolerance through the induction/activation of

261 e 4 T cell apoptosis during the induction of peripheral tolerance to a cross-presented self-Ag occurs

262 anism underlying the induction of CD8 T cell peripheral tolerance to a self-Ag expressed on pancreati

263 onses can be self-limiting in the context of peripheral tolerance to a self-antigen.

264 Peripheral tolerance to allergens is mediated in large p

265 This review focuses on mechanisms of peripheral tolerance to allergens with special emphasis

266 sinophils contributes to the construction of peripheral tolerance to allergens.

267 aimed at exploiting these pathways to induce peripheral tolerance to alloantigen.

268 the present model, we suggest that defective peripheral tolerance to an intestine-specific autoantige

269 the long-sought APC responsible for breaking peripheral tolerance to beta cell Ags in vivo.

270 this study, we evaluated the role of Treg in peripheral tolerance to composite tissue allografts (CTA

271 Peripheral tolerance to developmentally regulated antige

272 us vectors in C57BL/6 mice is able to induce peripheral tolerance to epitopes downstream of the PTC.

273 iently targeted the inflamed liver, restored peripheral tolerance to FTCD, and induced remission of A

274 Peripheral tolerance to liver autoantigens in AIH is par

275 sting of MUC1 vaccines revealed existence of peripheral tolerance to MUC1 that compromises their effi

276 establish a role for mast cells in mediating peripheral tolerance to myeloperoxidase, protecting them

277 tate, they participate in the maintenance of peripheral tolerance to self-antigens whereas under infl

278 l for T regulatory cells (Tregs) to maintain peripheral tolerance to self-antigens.

279 otic cells (ACs) in the steady state mediate peripheral tolerance to self-antigens.

280 ymic Treg cell generation is tuned to secure peripheral tolerance to self.

281 To study peripheral tolerance to skin-associated Ags, we generate

282 e well appreciated for their contribution to peripheral tolerance to tissue allografts, little is kno

283 ancer is often limited by the development of peripheral tolerance toward the dominant tumor-associate

284 ond to defined neoantigens in the context of peripheral tolerance, transplantation, autoimmune diseas

285 that SLOs are a primary site for maintaining peripheral tolerance under homeostatic conditions.

286 Induction of peripheral tolerance via sGARP is a promising potential

287 erived from iNKT cells is required to induce peripheral tolerance via the eye.

288 Conversely, induction of peripheral tolerance via the i.v. injection of PLP(139-1

289 te DCs in programming self-reactive CD4 cell peripheral tolerance was assessed by combining the CD11c

290 Peripheral tolerance was characterized by activation of

291 Peripheral tolerance was extremely efficient and complet

292 Peripheral tolerance was restored in F4/80(-/-) mice by

293 However, within the germinal center, peripheral tolerance was still enforced, and there was s

294 To elucidate the mechanisms controlling peripheral tolerance, we established two transgenic (Tg)

295 l strength is tightly coupled to central and peripheral tolerance, we examined whether Lyp620W impact

296 Because allogeneic MT is highly resistant to peripheral tolerance, we proposed to induce central tole

297 However, long-term survival and (dominant peripheral) tolerance were readily induced when DST was

298 e that furin is indispensable in maintaining peripheral tolerance, which is due, at least in part, to

299 4+FOXP3+ Tregs play key roles in maintaining peripheral tolerance, which is subject to regulation by

300 tive BCRs, N-RasD12 leads also to a break in peripheral tolerance with the production of autoantibodi