ライフサイエンスコーパス: self-tolerance

1 that initiate the disease cascade and break self tolerance.

2 Tight control of T(FH) numbers maintains self tolerance.

3 nt of the immune response and a guarantor of self tolerance.

4 le3-bearing DCs may be superior at breaching self tolerance.

5 een T cell subsets and have implications for self-tolerance.

6 roposed to impair Ag presentation and, thus, self-tolerance.

7 mmunological selection as a result of B cell self-tolerance.

8 to the generation and maintenance of B-cell self-tolerance.

9 tal role in the maintenance of immunological self-tolerance.

10 ritical regulators of immune homeostasis and self-tolerance.

11 ay a pivotal role in maintaining immunologic self-tolerance.

12 to protect from insulitis and fully restore self-tolerance.

13 o be critically involved in the induction of self-tolerance.

14 lial cells (mTECs) is essential to safeguard self-tolerance.

15 f apoptotic cells is crucial for maintaining self-tolerance.

16 major mechanism contributing to B lymphocyte self-tolerance.

17 tionship between thymic selection and immune self-tolerance.

18 e powerful immune reactions while preserving self-tolerance.

19 in regulating Breg function and maintaining self-tolerance.

20 ased susceptibility to infection and loss of self-tolerance.

21 trathymic constraints of differentiation and self-tolerance.

22 molecules and is thought to be important for self-tolerance.

23 f lymphocytes involved in the maintenance of self-tolerance.

24 al for immune homeostasis and maintenance of self-tolerance.

25 static clearing of ACs to maintain long-term self-tolerance.

26 (nTregs) are pivotal for the maintenance of self-tolerance.

27 ry T cells (Treg) are pivotal for peripheral self-tolerance.

28 Regulatory T cells (Treg) are crucial for self-tolerance.

29 ontrol adaptive immune responses and promote self-tolerance.

30 (+)Foxp3(+) cells are proven as essential to self-tolerance.

31 riphery that are critical for maintenance of self-tolerance.

32 ry T cells that are required for maintaining self-tolerance.

33 nTreg) cells are necessary for immunological self-tolerance.

34 an essential role in maintaining peripheral self-tolerance.

35 lls (Tregs) essential for the maintenance of self-tolerance.

36 ubset of CD4+ T cells needed for maintaining self-tolerance.

37 cal role in the maintenance of immunological self-tolerance.

38 t in preventing autoimmunity and the loss of self-tolerance.

39 (REG)), which play a key role in maintaining self-tolerance.

40 t CTLA-4 can act in trans to maintain T cell self-tolerance.

41 cal parameter for understanding the scope of self-tolerance.

42 a simple and effective approach to overcome self-tolerance.

43 urface expression, T cell growth arrest, and self-tolerance.

44 e responses as well as in the maintenance of self-tolerance.

45 trophenylalanine (pNO(2)Phe)-induced loss of self-tolerance.

46 anism to ensure establishing and maintaining self-tolerance.

47 the role of CD8 T cells in autoimmunity and self-tolerance.

48 y play a relevant role in the maintenance of self-tolerance.

49 hich prevent tissue inflammation and mediate self-tolerance.

50 PD-1/PD-L pathway is critical in maintaining self-tolerance.

51 unction of the immune mechanisms controlling self-tolerance.

52 n by infection can rapidly break established self-tolerance.

53 g that hyporesponsiveness is responsible for self-tolerance.

54 into the mechanism underlying restoration of self-tolerance.

55 e B cells escape the regulation that ensures self-tolerance.

56 for immune health, particularly to maintain self-tolerance.

57 lf from nonself in the periphery to maintain self-tolerance.

58 any of these lineages is sufficient to break self-tolerance.

59 (+)3(-)RANKL(+) inducer cells in intrathymic self-tolerance.

60 tenuating autoimmune responses and restoring self-tolerance.

61 suppression and are essential to maintaining self-tolerance.

62 mmune mechanisms that establish and maintain self-tolerance.

63 n inhibitors may have paradoxical effects on self-tolerance.

64 ntiation of autoreactive T cells to maintain self-tolerance.

65 s defining a novel mechanism for its role in self-tolerance.

66 s I molecules regulate NK cell responses and self-tolerance.

67 l role for these cells in maintaining immune self-tolerance.

68 ole in immune homeostasis and maintenance of self-tolerance.

69 anism for the establishment of immunological self-tolerance.

70 s essential for the establishment of central self-tolerance.

71 latory T cells (Tregs), the key mediators of self-tolerance.

72 plays a critical role in the maintenance of self-tolerance.

73 tatic programs balance immune protection and self-tolerance.

74 are critical for maintenance of immunologic self-tolerance.

75 ir nonredundant roles in the preservation of self-tolerance.

76 ory T cell (T reg) lineage, thus maintaining self-tolerance.

77 epertoire, and the importance this holds for self-tolerance.

78 novel targets that are more likely to evade self-tolerance.

79 entary roles of these two main mechanisms of self-tolerance.

80 g) play a crucial role in the maintenance of self-tolerance.

81 al role in RNA homeostasis and immunological self-tolerance.

82 icate balance between effective immunity and self-tolerance.

83 associated autoimmunity and thereby controls self-tolerance.

84 of the T cell repertoire is the induction of self-tolerance.

85 ntigen has an important role in establishing self-tolerance.

86 cells regulate immune responses and maintain self-tolerance.

87 to initiate negative selection and generate self-tolerance.

88 me of which are self-Ags and thus subject to self-tolerance.

89 This population has a role in maintaining self-tolerance, a transcriptome and an activation profil

90 ilar to PBC, suggesting that splenic loss of self-tolerance alone is sufficient to cause disease in t

91 s) by DCs is an important mechanism for both self tolerance and host defense.

92 ry cells (Tregs)) have a role in maintaining self tolerance and in regulating responses to infectious

93 is known about the mechanisms that maintain self tolerance and modulate anti-AChR Ab synthesis, AChR

94 regulatory (Treg) cells regulate peripheral self tolerance and possess the ability to suppress antit

95 + T cells that are essential for maintaining self tolerance and preventing autoimmunity, for limiting

96 age that is essential for the maintenance of self tolerance and prevention of murine autoimmune disea

97 gs) were named for their ability to maintain self tolerance and suppress T cell immunity.

98 Foxp3(+) regulatory T cells (Tregs) maintain self-tolerance and adoptive therapy, and using Foxp3(+)

99 umor models such as the A2xneu mice in which self-tolerance and aging are present at the same time ar

100 , we describe an animal tumor model in which self-tolerance and aging are present at the same time.

101 Tregs) are pivotal for maintenance of immune self-tolerance and also regulate immune responses to exo

102 crucial for the induction and maintenance of self-tolerance and are present in peripheral tissues suc

103 ism may be an effective means of reinforcing self-tolerance and attenuating autoimmunity.

104 P3+ Tregs are central for the maintenance of self-tolerance and can be defective in autoimmunity.

105 (r)) is the pivotal cell type that maintains self-tolerance and exerts active immune suppression.

106 s critical for the maintenance of peripheral self-tolerance and for down-regulation of immune respons

107 ccurring regulatory T cells (Tregs) maintain self-tolerance and function to suppress overly exuberant

108 (+) regulatory T (Treg) cells enforce immune self-tolerance and homeostasis, and variation in some as

109 tablishment and maintenance of immunological self-tolerance and homeostasis.

110 s), or efferocytosis, by DCs is critical for self-tolerance and host defense.

111 Self-tolerance and immune homeostasis are orchestrated b

112 atory T cells (Tregs) maintain immunological self-tolerance and immune homeostasis by suppressing abe

113 y T cells (Tregs) are critical regulators of self-tolerance and immune homeostasis.

114 ) cells are essential for the maintenance of self-tolerance and immune homeostasis.

115 ry T (Treg) cells are central to maintaining self-tolerance and immune homeostasis.

116 iscovered as immune suppressors critical for self-tolerance and immune homeostasis.

117 ls (Tregs) are central to the maintenance of self-tolerance and immune homeostasis.

118 cells (Tregs) are essential for maintaining self-tolerance and immune homeostasis.

119 T (Treg) cells are important in maintaining self-tolerance and immune homeostasis.

120 regulatory T cells (Tregs) are essential for self-tolerance and immune homeostasis.

121 egs) play a major role in the maintenance of self-tolerance and immune suppression, although the mech

122 Self-tolerance and immunity are actively acquired in par

123 cells suppress immune responses and control self-tolerance and immunity to pathogens, cancer, and al

124 NO(2)Phe) into autologous proteins overcomes self-tolerance and induces a long-lasting polyclonal IgG

125 (T(reg)) play a critical role in maintaining self-tolerance and inhibiting autoimmune disease.

126 r beta (TGFbeta) is important in maintaining self-tolerance and inhibits T cell reactivity.

127 checkpoint pathways, which normally maintain self-tolerance and limit collateral tissue damage during

128 r, detection of such epitopes is hampered by self-tolerance and limitations in the sensitivity of mas

129 f molecules normally involved in maintaining self-tolerance and limiting T cell responses, has emerge

130 reg) cells have crucial roles in maintaining self-tolerance and modulating adaptive immune responses.

131 eactive CD4 T cells is essential to maintain self-tolerance and prevent autoimmune disease.

132 he immune system is critical for maintaining self-tolerance and preventing autoimmunity.

133 ive thymocytes, is critical for establishing self-tolerance and preventing autoimmunity.

134 mmune cells and are critical for maintaining self-tolerance and preventing the development of autoimm

135 ls (mTECs) is essential for the induction of self-tolerance and prevents autoimmunity, with each TRA

136 itic cells and macrophages, preserves immune self-tolerance and prevents chronic inflammation and aut

137 tes the thymic display of PTAs that promotes self-tolerance and prevents organ-specific autoimmunity.

138 ical event that is alone sufficient to break self-tolerance and promote a CD8-mediated autoimmune res

139 sed as a key mechanism in the maintenance of self-tolerance and protection from type 1 diabetes.

140 al regulatory T cells (T reg cells) maintain self-tolerance and suppress autoimmune diseases such as

141 ulatory T cells (Treg) mediate immunological self-tolerance and suppress immune responses.

142 shown to play a crucial role in maintaining self-tolerance and suppressing autoimmunity.

143 (nTregs) are important for the induction of self-tolerance and the control of autoimmunity.

144 ranscription factor FoxP3 play a key role in self-tolerance and the control of inflammation.

145 that may, in turn, contribute to the loss of self-tolerance and the development of autoimmunity.

146 a root cause of the progressive breakdown of self-tolerance and the development of diabetes in nonobe

147 eady-state cell apoptosis is associated with self-tolerance and the need for developing a more practi

148 ent co-inhibition can lead to a breakdown of self-tolerance and thus to autoimmunity.

149 beta) suppresses T cell function to maintain self-tolerance and to promote tumor immune evasion.

150 important for the maintenance of intestinal self-tolerance and will likely prove to be an important

151 d in the normal environment, so as to ensure self-tolerance and yet optimize sensitivity to changes i

152 t processes necessary for the enforcement of self-tolerance, and both require high-affinity interacti

153 olecules is central to antigen presentation, self-tolerance, and CD8(+) T-cell activation.

154 ew findings for the clonal selection theory, self-tolerance, and immunodominance are discussed.

155 a key role in the maintenance of peripheral self-tolerance, and it has been suggested that diabetes-

156 lymphoid tissue formation, breach of humoral self-tolerance, and salivary hypofunction after delivery

157 g) cells are important in the maintenance of self-tolerance, and the depletion of Treg cells correlat

158 crossroads of innate and adaptive immunity, self-tolerance, and tissue homeostasis.

159 However, mechanisms that sustain self-tolerance are poorly understood.

160 cal role for these costimulatory pathways in self-tolerance as well as thymic epithelial development.

161 tory T cells (Tregs) play a critical role in self-tolerance, as seen in murine autoimmunity.

162 ion of self antigens and favors diversity of self-tolerance between individuals.

163 cells) suppress immune responses to maintain self tolerance, but they also protect cancerous tissues.

164 lls) are required for immune homeostasis and self-tolerance, but must be stringently controlled to pe

165 ted effector Tregs (eTregs) are required for self-tolerance, but the heterogeneity and relationships

166 of autoreactive thymocytes is important for self-tolerance, but the intrathymic signals that induce

167 y receptor CTLA-4 is critical in maintaining self-tolerance, but the mechanisms of its actions have r

168 cells (T reg) are essential for maintaining self-tolerance, but their functional mechanisms and site

169 ntion of autoimmunity and the maintenance of self-tolerance, but these cells also have an active role

170 lls) modulate the immune system and maintain self-tolerance, but whether they affect haematopoiesis o

171 ccurring regulatory T cells (Tregs) maintain self tolerance by dominant suppression of potentially se

172 out by the presence of Tregs, which maintain self-tolerance by directly inhibiting T cells, NK cells,

173 an important role in maintaining peripheral self-tolerance by discriminating self from nonself in hu

174 mic epithelium alone is capable of promoting self-tolerance by eliminating autoreactive CD4 single-po

175 lized subset of CD4(+) T cells that maintain self-tolerance by functionally suppressing autoreactive

176 osis in dendritic cells (DCs) helps regulate self-tolerance by generating transgenic mice expressing

177 tor plays an important role in immunological self-tolerance by mediating the ectopic expression of pe

178 Thymic dendritic cells (DC) mediate self-tolerance by presenting self-peptides to and deplet

179 regs, Tim-1 is also critical for maintaining self-tolerance by regulating IL-10 production in Bregs.

180 ant role in the maintenance of immunological self-tolerance by suppressing immune responses against a

181 B lymphocyte compartment for acquisition of self-tolerance can be harnessed to induce humoral unresp

182 Consistent with defective self-tolerance, CD33/LAIR-1 expression is reduced in sys

183 ment of ANA and underscore the importance of self-tolerance checkpoints at the postmutational stage o

184 Loss of self-tolerance contributes to pulmonary vascular remodel

185 n unresponsiveness to self (a state known as self-tolerance) contributes to the development of autoim

186 ntigens, providing evidence that the loss of self-tolerance during acute GVHD leads to the emergence

187 s of B cell selection and the maintenance of self-tolerance during early and adult life.

188 lays important roles in antigen sampling and self-tolerance during infection and inflammation.

189 c cells is essential to prevent breakdown of self-tolerance ensuing from aberrant detection of endoge

190 But how is self-tolerance first broken to initiate this loop?

191 cells, which maintain immune homeostasis and self-tolerance, form an immunological synapse (IS) with

192 cells (Tregs) as regulators of immunological self-tolerance has stimulated tremendous interest in the

193 of imbalanced immune homeostasis and loss of self-tolerance have been identified as common to multipl

194 ells and molecules involved in the breach of self-tolerance have been partially defined in experiment

195 T cells have revealed several mechanisms of self-tolerance; however, which mechanisms operate in nor

196 ude that overall, GITR stimulation overcomes self-tolerance/ignorance and enhances T cell-mediated an

197 s on: (i) T cell tolerance to self-antigens (self-tolerance); (ii) T cell exhaustion during chronic i

198 n, an effect important to the maintenance of self-tolerance, immune suppression, and tumor immunosurv

199 in serum prolactin levels induce a break in self tolerance in mice with a BALB/c genetic background.

200 elicit productive TLR activation, and break self-tolerance in anergic DNA-reactive B cells.

201 Reestablishing self-tolerance in autoimmunity is thought to depend on s

202 une disorder characterized by a breakdown of self-tolerance in B cells and the production of antibodi

203 Induction of self-tolerance in developing T cells depends on medullar

204 oints and mechanisms that enforce a state of self-tolerance in developing T cells specific for BCR V

205 ithelial cells (MECs), driving immunological self-tolerance in differentiating T cells.

206 ate a Th repertoire that is unconstrained by self-tolerance in K-negative individuals.

207 contribution of NEIL3 to the maintenance of self-tolerance in Neil3-/- mice.

208 The results demonstrate that the defect in self-tolerance in NZB AIHA is directed to the RBC type,

209 defects in Tregs contribute to breakdown of self-tolerance in patients with chronic ITP.

210 play a role in the breakdown of immunologic self-tolerance in patients with SLE.

211 repertoire that contributes to breakdown of self-tolerance in primary biliary cirrhosis, whereas tho

212 BCMA works to control B cell homeostasis and self-tolerance in systemic autoimmunity.

213 ells and plasmablasts contributes to loss of self-tolerance in systemic lupus erythematosus (SLE).

214 subjects lacking the AIRE gene, critical for self-tolerance in T lymphocytes, show a broad range of a

215 for therapies able to restore euglycemia and self-tolerance in T1DM.

216 mains unclear whether they influence loss of self-tolerance in the adaptive immune compartment.

217 ets-1 levels is essential to prevent loss of self-tolerance in the B cell compartment.

218 in vivo and was required for maintenance of self-tolerance in the murine model of pristane-induced l

219 f T-cell activation and the establishment of self-tolerance in the periphery.

220 dditional factors are required for breaching self-tolerance in the setting of lymphopenia.

221 Establishment of self-tolerance in the thymus depends on promiscuous expr

222 The development of T-cell self-tolerance in the thymus is important for establishi

223 Acquisition of self-tolerance in the thymus requires T cells to discrim

224 medullary epithelium and for maintenance of self-tolerance in thymocyte development.

225 ive or deleterious effects on loss of B cell self-tolerance in vivo, we depleted neutrophils at diffe

226 ge, and whether T(reg) cells are critical in self-tolerance in wild-type mice remains unknown.

227 cells are indispensable to the breakdown of self-tolerance, in contrast to B cells which play a more

228 e implicated in the regulation of peripheral self-tolerance induction.

229 c epithelial cells and, thus, the control of self-tolerance induction.

230 in the host thymus implying an impairment in self-tolerance induction.

231 Breakdown in self-tolerance is caused, in part, by loss of regulatory

232 Self-tolerance is induced and sustained by central and p

233 the chimeric subjects have, suggesting that self-tolerance is induced in addition to tolerance to al

234 ular antigens expressed on ACs; however, how self-tolerance is maintained is not well understood.

235 to uncouple anti-tumor activity from loss of self-tolerance is necessary to increase the therapeutic

236 sclerosis and type-1 diabetes, dysfunctional self-tolerance is partially mediated by a population of

237 e achieving tumor rejection while preserving self-tolerance is particularly important for the central

238 R diversity of T regulatory (Treg) cells for self-tolerance is poorly understood.

239 T cell self-tolerance is thought to involve peripheral toleranc

240 ance of T cell homeostasis and immunological self-tolerance later in life.

241 modification of protein by drugs may disrupt self-tolerance, leading to lymphocyte activation.

242 Because of mechanisms of self-tolerance, many tumor-specific CD8 T cells exhibit

243 regulatory mechanisms that maintain or break self-tolerance may lead to new strategies for the treatm

244 Clonal anergy is an enigmatic self-tolerance mechanism because no apparent purpose is

245 tein, specific CD8(+) T cells are subject to self-tolerance mechanisms and typically exhibit only mod

246 recent studies advance our understanding of self-tolerance mechanisms at work in NK cells.

247 ely, AIR may be associated with dysregulated self-tolerance mechanisms in the thymus.

248 B cells is normally limited by a variety of self-tolerance mechanisms, including clonal deletion, an

249 en model for their ability to trigger thymic self-tolerance mechanisms.

250 ortant implications for understanding T cell self-tolerance mechanisms.

251 How can such T cells escape self-tolerance mechanisms?

252 at MerTK plays a critical role in regulating self-tolerance mediated between ACs, DCs, and T cells.

253 a likely contributing factor in the loss of self-tolerance observed in type 1 diabetes (T1D).

254 Peripheral mechanisms of self-tolerance often depend on the quiescent state of th

255 Mechanisms of self-tolerance often result in CD8(+) tumor-infiltrating

256 (Aire) gene have revealed that Aire promotes self-tolerance partly by inducing the transcription of a

257 These data suggest that the NK cell self-tolerance process dynamically modulates the NK cell

258 play an important role in the maintenance of self-tolerance, proliferate poorly and fail to produce I

259 ms underpinning such HLA-mediated effects on self-tolerance remain unclear.

260 The relevance of this diversity to maintain self-tolerance remains unknown.

261 The maintenance of immunologic self-tolerance requires the coordination of multiple com

262 Furthermore, GVHD results in the breaking of self tolerance, resulting in the emergence of donor T ce

263 may falter, culminating in the breakdown of self-tolerance, resulting in immune-mediated attack dire

264 (Tregs) are essential for the maintenance of self-tolerance, significant interest surrounds the devel

265 the thymus results in deletion and promotes self-tolerance, such recognition by mature T cells in th

266 lymphocytes is not alone sufficient to break self-tolerance, suggesting the involvement of other cell

267 e system involves mechanisms that ensure the self-tolerance, survival and quiescence of hematopoietic

268 ring TIL hypofunction more closely resembled self-tolerance than viral exhaustion.

269 a cost of insufficient development of immune self-tolerance that favors the production of GAD65 autoa

270 at normally maintains B cell homeostasis and self-tolerance through limited production.

271 understood in the thymus, where it promotes self-tolerance through tissue-specific antigen (TSA) exp

272 f apoptosis and anergy to the maintenance of self-tolerance to a systemic Ag.

273 f dying cells, as well as the maintenance of self-tolerance to AC-derived autoantigens.

274 results illustrate the importance of NK cell self-tolerance to activated CD8+ T cells and demonstrate

275 toimmune diseases result from a breakdown in self-tolerance to autoantigens.

276 y with pathogen-derived antigens might break self-tolerance to induce autoimmune disease.

277 eate vaccines against pathogens and to break self-tolerance to initiate an immune response to dysfunc

278 Innate immune signals help break self-tolerance to initiate autoimmune diseases such as t

279 bone marrow-derived cells establishes robust self-tolerance to islet autoantigens and is sufficient t

280 Self-tolerance to melanocyte differentiation Ags limits

281 y fundamental immune processes, ranging from self-tolerance to pathogen immunity, interleukin (IL)-2

282 important mechanism enforcing immunological self-tolerance to prevent inappropriate activation of T

283 ary biliary cirrhosis is breakdown of T-cell self-tolerance to pyruvate dehydrogenase complex (PDC).

284 but whether they play a role in maintaining self-tolerance under steady-state conditions is not know

285 A breakdown in self-tolerance underlies autoimmune destruction of beta-

286 ctions, which mediate negative selection and self-tolerance, upregulate expression of LTalpha, LTbeta

287 Receptor editing is a mechanism of self-tolerance used in newly generated B cells.

288 f the MHCII self-peptide repertoire mediates self tolerance, we generated NOD mice that constitutivel

289 In RS mutant mice, receptor editing and self-tolerance were impaired, in some cases leading to a

290 CCX-CKR(-/-) mice, suggestive of a defect in self-tolerance when CCX-CKR is deleted.

291 -4 is a key immune checkpoint in maintaining self-tolerance, which can be co-opted by cancer to evade

292 re educated by MHC class I ligands to ensure self-tolerance while also promoting lytic competency aga

293 ry immunoreceptor that is a key regulator of self-tolerance with established genetic associations to

294 knockout mice, dual knockout mice abrogated self-tolerance with resultant autoimmune infiltrates in

295 (CTLA-4; CD152) is of pivotal importance for self-tolerance, with deficiency or unfavorable polymorph

296 ith pulmonary hypertension, and that loss of self-tolerance would result in production of pathologic

297 y permits the system to safeguard peripheral self tolerance yet promote the capacity to deal with for

298 antigen is central to adaptive immunity and self-tolerance, yet how this is determined by different

299 cells (LNSCs) closely regulate immunity and self-tolerance, yet key aspects of their biology remain

300 a pivotal role in maintaining immunological self-tolerance; yet, excessive Treg cell activities supp