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 lection are central to adaptive immunity and self-tolerance.

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

6 icate balance between effective immunity and self-tolerance.

7 associated autoimmunity and thereby controls self-tolerance.

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

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

10 cells regulate immune responses and maintain self-tolerance.

11 to initiate negative selection and generate self-tolerance.

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

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

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

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

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

17 nd thus eliminated through the mechanisms of self-tolerance.

18 ritical regulators of immune homeostasis and self-tolerance.

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

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

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

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

23 major mechanism contributing to B lymphocyte self-tolerance.

24 tionship between thymic selection and immune self-tolerance.

25 e powerful immune reactions while preserving self-tolerance.

26 in regulating Breg function and maintaining self-tolerance.

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

28 trathymic constraints of differentiation and self-tolerance.

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

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

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

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

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

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

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

36 ontrol adaptive immune responses and promote self-tolerance.

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

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

39 roles in maintaining immune homeostasis and self-tolerance.

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

41 ily TAM (Tyro3, Axl, and MerTK), to maintain self-tolerance.

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

43 an essential role in maintaining peripheral self-tolerance.

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

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

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

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

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

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

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

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

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

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

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

55 on and maintenance of immune homeostasis and self-tolerance.

56 anism to ensure establishing and maintaining self-tolerance.

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

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

59 hich prevent tissue inflammation and mediate self-tolerance.

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

61 unction of the immune mechanisms controlling self-tolerance.

62 thymus, a process important for establishing self-tolerance.

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

64 into the mechanism underlying restoration of self-tolerance.

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

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

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

68 (+)3(-)RANKL(+) inducer cells in intrathymic self-tolerance.

69 tenuating autoimmune responses and restoring self-tolerance.

70 suppression and are essential to maintaining self-tolerance.

71 mmune mechanisms that establish and maintain self-tolerance.

72 tatic programs balance immune protection and self-tolerance.

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

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

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

76 g that hyporesponsiveness is responsible for self-tolerance.

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

78 defense against pathogens while maintaining self-tolerance.

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

80 are critical for maintenance of immunologic self-tolerance.

81 se by suppressing inflammation and promoting self-tolerance.

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

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

84 T cell responses in cancer and contribute to self-tolerance.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 atory T cells (nTregs) ensure the control of self-tolerance and are currently used in clinical trials

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

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

102 cine strategies are required to vanquish the self-tolerance and elicit robust immune responses agains

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

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

105 oimmune disease characterised by the loss of self-tolerance and formation of nuclear autoantigens and

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

107 are necessary for the maintenance of immune self-tolerance and homeostasis(1,2).

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

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

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

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

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

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

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

120 T (Treg) cells are important in maintaining 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 latory T cells (T(regs)) maintain peripheral self-tolerance and limit immune mediated pathology.

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

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

131 In rheumatoid arthritis (RA), breakdown of self-tolerance and onset of clinical disease are separat

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

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 he mechanisms that underpin the breakdown in self-tolerance and propagation of autoimmune responses.

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

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

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

143 shown to play a crucial role in maintaining self-tolerance and suppressing 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 a key regulator of pregerminal center B cell self-tolerance and thus represents a druggable pathway t

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 B cells must actively undergo selection for self-tolerance before maturing into their resting follic

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

163 ulatory T cells (T(reg) cells) maintain host self-tolerance but are a major barrier to effective canc

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

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

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

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

168 positive selection and the establishment of self-tolerance, but the mechanisms controlling their fet

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

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

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

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

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

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

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

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

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

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

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

180 ntly, CTL activated in this manner can break self-tolerance by reacting to self-peptides presented by

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

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

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

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

185 standing of how self-reactive B cells escape self-tolerance checkpoints to secrete pathogenic autoant

186 Loss of self-tolerance contributes to pulmonary vascular remodel

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

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

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

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

191 Autoimmunity can occur when a checkpoint of self-tolerance fails.

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

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

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

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

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

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

198 ual framework to understand the breakdown of self-tolerance, if such modifications occur in a tissue-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 dy describes a newly discovered mechanism of self-tolerance induced by the intravenous delivery of a

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

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

231 Regulatory T (Treg) cells control self-tolerance, inflammatory responses and tissue homeos

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 Characterizing self-tolerance mechanisms and their failure is critical

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

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

249 However, examination of self-tolerance mechanisms has relied primarily on transg

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

251 s retrogenic model can be employed to define self-tolerance mechanisms restricting T and B cell respo

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

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

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

255 n with implications for understanding T cell self-tolerance mechanisms.

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

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

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

259 ial for providing and maintaining peripheral self-tolerance of potentially autoreactive cells.

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

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

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

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

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

265 ve lymphocytes, yet how this lineage attains self-tolerance remains unknown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ies for type 1 diabetes (T1D) should restore self-tolerance without inducing chronic immunosuppressio

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

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