ライフサイエンスコーパス: self-reactive

1 nsure that self-reactive T cells are not too self-reactive.

2 that disease-associated IgG4 antibodies are self-reactive.

3 cleobase substrates in this approach are not self-reactive, a base-filling approach may reduce the fo

4 e of the CNS that is mediated, in part, by a self-reactive Ab against the astrocyte aquaporin-4 prote

5 that functional tyrosine sulfation occurs in self-reactive Abs and suggest a potential new mechanism

6 sent a higher serum level of natural Igs and self-reactive Abs.

7 CD25(hi) (Triple(hi)) Treg cells were highly self-reactive and controlled lympho-proliferation in per

8 BV(+) memory B cells express lower levels of self-reactive and especially polyreactive antibodies tha

9 o)CD25(lo) (Triple(lo)) Treg cells were less self-reactive and limited the development of colitis by

10 ction of IgG-positive memory B cells express self-reactive and polyreactive IgG antibodies that frequ

11 Self-reactive antibodies and parasite-specific IgG in fe

12 t mice produced high amounts of low-affinity self-reactive antibodies and showed significant lymphocy

13 tibodies, which have shown that nonspecific, self-reactive antibodies are rich in Arg and other posit

14 ntibody self/non-self discrimination discard self-reactive antibodies before they can be tested for b

15 In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus ne

16 The occurrence of self-reactive antibodies correlated with overall antibod

17 0) is an autoimmune disease characterized by self-reactive antibodies resulting in systemic inflammat

18 ferentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis

19 nondonor HLA specific antibodies (NDSA) and self-reactive antibodies that develop alongside donor-sp

20 gene segment encodes in humans intrinsically self-reactive antibodies that recognize I/i carbohydrate

21 However, in females, the presence of self-reactive antibodies was positively associated with

22 pid response that includes the production of self-reactive antibodies.

23 t and thus is not involved in the editing of self-reactive antibodies.

24 d associations between fitness and heritable self-reactive antibody responsiveness in a wild populati

25 Yet, not everyone who developes self-reactive autoantibodies will manifest autoimmune di

26 ls, we have limited mechanistic insight into self-reactive autoimmune T cell development and their es

27 in suppressing the spontaneous activation of self-reactive B and T cells during lupus.

28 in T cells prevented Tfh cell accumulation, self-reactive B cell activation, and autoantibody produc

29 B cell follicles to prevent the expansion of self-reactive B cell clones.

30 lator), a cytokine that promotes survival of self-reactive B cell clones.

31 These results support the generation of self-reactive B cell repertoires during the autoimmune p

32 a provide insight into the maturation of the self-reactive B cell response, contextualizing the epito

33 important role of Act1 in the regulation of self-reactive B cells and reveal how Act1 functions to p

34 ngage a deletional checkpoint for removal of self-reactive B cells and selectively kill ALL cells.

35 Some self-reactive B cells are able to escape these checkpoin

36 Self-reactive B cells are eliminated during development

37 Self-reactive B cells are generally removed by receptor

38 r editing is important for understanding how self-reactive B cells are regulated.

39 central tolerance is a process through which self-reactive B cells are removed from the B cell repert

40 t help to distinguish self-reactive from non-self-reactive B cells at four distinct checkpoints.

41 ed on FDCs mediates effective elimination of self-reactive B cells at the transitional stage.

42 However, selection of self-reactive B cells by Ag on FDCs has not been address

43 tible genetic backgrounds with the rescue of self-reactive B cells by T cells allows the generation o

44 Autoantibodies develop when self-reactive B cells escape the regulation that ensures

45 inal centers (GCs) in lymphoid tissues where self-reactive B cells expand and differentiate.

46 Checkpoints are in place to prevent self-reactive B cells from further development and activ

47 Pathogenic autoantibodies, arising from self-reactive B cells having undergone somatic hypermuta

48 Self-reactive B cells in BALB/c AM14 transgenic (Tg) rhe

49 erves an important role in the activation of self-reactive B cells in systemic autoimmunity.

50 Although the negative selection of self-reactive B cells in the bone marrow of mammals has

51 ight be an important mechanism through which self-reactive B cells might successfully revise their in

52 Self-reactive B cells not controlled by receptor editing

53 Notwithstanding, some self-reactive B cells persist beyond this checkpoint, sh

54 e mechanisms that prevent the development of self-reactive B cells remain incompletely understood.

55 clones were newly generated B cells and not self-reactive B cells that had escaped depletion and rep

56 competent peripheral B cell pool limited in self-reactive B cells that may produce pathogenic autoan

57 MYD88(L265P) caused self-reactive B cells to accumulate in vivo only when ap

58 results in B cell hyperactivity, survival of self-reactive B cells, and differentiation to autoantibo

59 n FDCs and to monitor the fate of developing self-reactive B cells.

60 s a critical physiologic mechanism to sensor self-reactive B cells.

61 efective B cell selection and elimination of self-reactive B cells.

62 e generation, activation, and persistence of self-reactive B cells.

63 ar to be less frequently used to edit/revise self-reactive B cells.

64 orchestrating secondary Ig rearrangements in self-reactive B cells.

65 s critical for suppressing the activation of self-reactive B cells; however, the mechanism underlying

66 ment and subsequent long-term maintenance of self-reactive B-1 B cells.

67 tionally equivalent to acute activation of a self-reactive BCR on ALL cells.

68 B cells from elimination by diluting out the self-reactive BCR through the expression of a second inn

69 hyperactivation above maximum (for example, self-reactive BCR) thresholds of signalling strength cau

70 a response to inappropriate signaling from a self-reactive BCR, or as part of a stochastic mechanism

71 onfunctional IgH genes or IgH genes encoding self-reactive BCRs and contributes to the diversificatio

72 figuration, express low-affinity, poly-, and self-reactive BCRs.

73 e B-cell receptor (BCR) repertoire including self-reactive BCRs.

74 can be induced from pre-existing, residual, self-reactive BnAb-expressing B cells in vivo using a st

75 The inappropriate expansion of self-reactive "bystander" T cells can contribute to auto

76 a-light-chain+ naive B cells, development of self-reactive CD11c+FAS+ B cells, and evidence for spont

77 the role of steady state DCs in programming self-reactive CD4 cell peripheral tolerance was assessed

78 In contrast, when mature self-reactive CD4 cells encounter their cognate epitopes

79 ted by MHC class II molecules and shapes the self-reactive CD4 T cell repertoire.

80 Self-reactive CD4 T cells are thought to have a central

81 ht into the role of TSSP in the selection of self-reactive CD4 T cells by endogenous self-Ags, we exa

82 d the elaborate Treg-dependent regulation of self-reactive CD4(+) T cell proliferation within the CNS

83 Self-reactive CD4(+) T cells are major drivers of autoim

84 Furthermore, self-reactive CD4(+) T cells that expanded in the presen

85 ognition of systemic Ag induces tolerance in self-reactive CD4(+) T cells, but induction of CD40 sign

86 gning immunotherapies that incorporate tumor/self-reactive CD4(+) T cells.

87 Of interest, the self-reactive CD4(+) Tconvs and Tregs displayed overlapp

88 of acquired TTP by stimulating low-affinity, self-reactive CD4+ T cells.

89 We also show that DN T cells derived from self-reactive CD8 cells express the inhibitory molecules

90 To explore whether self-reactive CD8 T cells could attack CNS neurons in vi

91 This work reveals the complex regulation of self-reactive CD8 T cells in vitiligo and demonstrates t

92 nity by inducing MHC-I-dependent deletion of self-reactive CD8(+) T cells and MHC-II-dependent anergy

93 There is compelling evidence that self-reactive CD8(+) T cells are a major factor in devel

94 lls (LNSCs), have been described to tolerize self-reactive CD8(+) T cells in LNs.

95 rcumvent this problem, and given the role of self-reactive CD8(+) T cells in the development of type

96 B cells engage self-reactive CD8(+) T cells in the pancreatic lymph nod

97 conditions like type 1 diabetes to progress, self-reactive CD8(+) T cells would need to interact with

98 ith monotherapy, elicits high frequencies of self-reactive CD8(+) T cells, potent tumor-specific CD8(

99 levant specificity, blunted the expansion of self-reactive CD8(+) T cells, suggesting B-cell antigen

100 diabetes by cross-presenting autoantigen to self-reactive CD8(+) T cells.

101 T cells to adopt the phenotype of their less self-reactive cell-counterparts.

102 hen CD8 T cells from repertoires enriched in self-reactive cells (Aire-deficient) are transferred int

103 in a specialized organ, the thymus, in which self-reactive cells are either eliminated or differentia

104 The self-reactive cells initially exhibited effector activit

105 oreactive heavy chain, we show enrichment in self-reactive cells specifically at the transitional to

106 ny stages of thymocyte development, allowing self-reactive cells to escape clonal deletion; reducing

107 toll in the form of pathologies mediated by self-reactive cells.

108 hought to be attributable to the deletion of self-reactive cells.

109 the expression of PD-1 and Helios, represent self-reactive cells.

110 ty, immunological memory, and elimination of self-reactive clones (2).

111 -1(+) IELp population included more strongly self-reactive clones and was largely restricted by class

112 vides the evidence that complete deletion of self-reactive clones is rare.

113 e B cells from WAS patients were enriched in self-reactive clones, revealing that peripheral B cell t

114 a substantial proportion of polyreactive and self-reactive clonotypes, suggesting that activation che

115 ) use a distinct TCR repertoire and are more self-reactive compared with conventional T cells.

116 taneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in second

117 ulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues.

118 ovel mechanism that prevents accumulation of self-reactive cytotoxic effectors, highlighting the impo

119 esponses by CD4(+) T cells, likely driving a self-reactive disease process.

120 during acute GVHD leads to the emergence of self-reactive donor T cells that are capable of recogniz

121 B7-1 pathway inhibits potentially pathogenic self-reactive effector CD4(+) and CD8(+) T cell response

122 maintain peripheral tolerance by suppressing self-reactive effector T cells.

123 o protect the organism against autoimmunity, self-reactive effector/memory T cells (T(E/M)) are contr

124 hat the T cell repertoire is in fact broadly self-reactive, even self-centered.

125 , or apoptosis, and that help to distinguish self-reactive from non-self-reactive B cells at four dis

126 e through failure of FAS-mediated removal of self-reactive germinal center (GC) B cells.

127 lls is associated with positive selection of self-reactive germinal center B cells and autoimmunity i

128 Using a biomarker to track a self-reactive H chain in peripheral blood, we found evid

129 that can be used to predict whether TCRs are self-reactive have not been fully elucidated.

130 By following the fate of self-reactive human kappa(+) B cells relative to nonauto

131 recent reports describing the prevalence of self-reactive IgE and discuss novel findings that incrim

132 The presence of circulating self-reactive IgE in patients with autoimmune disorders

133 Collectively, these results indicate that self-reactive IgE is produced during malaria.

134 , the negative correlation between levels of self-reactive IgE to 14-3-3 epsilon protein and parasite

135 duals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express

136 The presence of self-reactive IgG autoantibodies in human sera is largel

137 In normal mice, self-reactive IgG2a-switched B cells were deleted, leadi

138 Self-reactive IgGs contribute to the pathology of autoim

139 We investigate the role of self-reactive IgM in the unique setting of transplantati

140 y-deficient mice reconstituted with specific self-reactive IgM monoclonal antibodies, we identified n

141 sis patients also contained polyreactive and self-reactive IgM.

142 undamental and unanticipated role in purging self-reactive immature and transitional B cells during t

143 and could be involved in receptor editing of self-reactive immature B cells.

144 hrough its RAG-coupled genotoxic activity in self-reactive immature B cells.

145 ent in the thymus, deletion of high-affinity self-reactive immature thymocytes contributes to toleran

146 )) play a critical role in the inhibition of self-reactive immune responses and as such have been imp

147 ing Ab (bnAb) 2F5 has been shown to be poly-/self-reactive in vitro, and we previously demonstrated t

148 Self-reactive, innate-like B cells contact and are selec

149 es may be caused, in part, by low numbers of self-reactive lymphocytes surviving negative selection.

150 f the mechanisms that maintain inactivity of self-reactive lymphocytes.

151 y is defective elimination and/or control of self-reactive lymphocytes.

152 Using a series of polyclonal and transgenic self-reactive models harboring the analogous mutation in

153 demyelinating disease of the CNS mediated by self-reactive, myelin-specific T cells.

154 er the association between the production of self-reactive NAbs and NAbs that afford protection again

155 indings indicate that although production of self-reactive NAbs can be independent of germline D(H) s

156 n vivo calcineurin inhibition leads the most self-reactive naive CD4 T cells to adopt the phenotype o

157 at are optimized for the selection of weakly self-reactive, naive T-cell clones.

158 Self-reactive natural Abs initiate injury following isch

159 ly conserved MPER is a target of potent, non-self-reactive neutralizing antibodies, suggesting that H

160 unoglobulin heavy chain (IgH) genes encoding self-reactive or mono-specific antibodies or non-functio

161 T cells prevents the harmful accumulation of self-reactive pathogenic T cells in vital organs.

162 is difficult to assess the entire contained self-reactive peripheral T cell repertoire in healthy in

163 that mimics can induce the expansion of new self-reactive populations not initially present in the p

164 ells (Tregs) and enriches this repertoire in self-reactive receptors, contributing to its vast divers

165 ance in autoimmunity is thought to depend on self-reactive regulatory T cells (Tregs).

166 rtant to explore whether T cells known to be self-reactive (regulatory T cells) or those involved in

167 A truncated self-reactive repertoire, devoid of high-avidity T cells

168 CD5(low) T cell pool showed that the overall self-reactive response has not only a diverse polyclonal

169 negative selection of superantigen-specific, self-reactive, single-positive thymocytes, and we show t

170 chain usage and enrichment for low-affinity self-reactive specificities in murine marginal zone and

171 B cell development, promoting enrichment of self-reactive specificities into the follicular mature c

172 e the emerging T cell receptor repertoire of self-reactive specificities.

173 However, purging of immature and mature self-reactive T and B cells is incomplete and may also r

174 pply to autoimmune diseases involving clonal self-reactive T and B lymphocytes--a process referred to

175 2D affinity measurements of three of these self-reactive T cell clones demonstrated a normal off-ra

176 formation of immunological synapses (IS) in self-reactive T cell clones from patients with multiple

177 Self-reactive T cell clones that escape negative selecti

178 the T cell repertoire but does not eliminate self-reactive T cell clones.

179 ed that even the naive T cell pool contained self-reactive T cell precursors.

180 Multiple studies highlighted the overtly self-reactive T cell repertoire in the diabetes-prone NO

181 Thus, the self-reactive T cell repertoire is controlled by overlap

182 Because the peripheral self-reactive T cell repertoire is devoid of high-avidit

183 its ligands in regulating antimicrobial and self-reactive T cell responses and discuss the therapeut

184 of the PD-L1:B7-1 interaction in regulating self-reactive T cell responses is not yet clear.

185 dicate two checkpoints where PD-1 attenuates self-reactive T cell responses: presentation of self-Ag

186 The self-reactive T cells also maintained a high degree of m

187 fector T cells and controls the expansion of self-reactive T cells and development of autoimmune dise

188 up new avenues to evaluate the repertoire of self-reactive T cells and its role in onset of diabetes.

189 importance of Foxp3(+) Tregs in controlling self-reactive T cells and preventing autoimmunity is wel

190 tributing to a reduction in the frequency of self-reactive T cells and resistance to autoimmunity.

191 eloping thymocytes, resulting in deletion of self-reactive T cells and supporting regulatory T cell d

192 Activation of self-reactive T cells and their trafficking to target ti

193 ion of abundant cytokine mRNAs is limited in self-reactive T cells and, thus, identify posttranscript

194 uster of differentiation 1c (CD1c)-dependent self-reactive T cells are abundant in human blood, but s

195 However, if these mechanisms fail, self-reactive T cells are activated and autoimmune respo

196 Although many self-reactive T cells are eliminated by negative selecti

197 How self-reactive T cells are kept functionally inactive is,

198 echanism of central tolerance to ensure that self-reactive T cells are not too self-reactive.

199 However, it remains unknown how peripheral self-reactive T cells are specifically instructed to bec

200 Research into how self-reactive T cells are tolerized in lymph nodes has f

201 ought to be an autoimmune condition in which self-reactive T cells attack insulin-secreting pancreati

202 sclerosis is an autoimmune disease in which self-reactive T cells attack oligodendrocytes that myeli

203 responses: presentation of self-Ag to naive self-reactive T cells by dendritic cells in the draining

204 ry thymic epithelial cells (mTECs) eliminate self-reactive T cells by displaying a diverse repertoire

205 It has been shown that self-reactive T cells can be detected in the periphery.

206 Thus, self-reactive T cells can become pathogenic in the targe

207 Self-reactive T cells can escape thymic deletion and the

208 effective systems and conclude that slightly self-reactive T cells can exist within the immune system

209 All self-reactive T cells contained a large number of phosph

210 The failure to eliminate self-reactive T cells during negative selection is a pre

211 of autoimmunity requires the elimination of self-reactive T cells during their development and matur

212 of autoimmunity requires the elimination of self-reactive T cells during their development in the th

213 TCR repertoire enables Treg cells to control self-reactive T cells effectively, especially when thymi

214 enable acquisition of effector functions by self-reactive T cells encountering large amounts of self

215 facilitate escape from negative selection by self-reactive T cells encountering very small amounts of

216 or negative selection, sufficient numbers of self-reactive T cells escape deletion and create an incr

217 lity to generate effector cytokine proteins, self-reactive T cells express large amounts of cytokine

218 d issue in immune tolerance is what prevents self-reactive T cells from activation.

219 Individual self-reactive T cells have been discovered in both human

220 cells may play an important role in keeping self-reactive T cells in check.

221 rance by dominant suppression of potentially self-reactive T cells in peripheral tissues.

222 When potentially self-reactive T cells in the periphery were activated, t

223 ng lymph node and reactivation of pathogenic self-reactive T cells in the target organ.

224 herefore, regulates the early development of self-reactive T cells in the thymus and plays a key role

225 nological tolerance requires the deletion of self-reactive T cells in the thymus.

226 uses expressing OVA-peptide variants induced self-reactive T cells in vivo that matured into memory T

227 ection occurs because potentially pathogenic self-reactive T cells included in the pool of intermedia

228 pression may provide a potential therapy for self-reactive T cells involved in autoimmune diseases th

229 Because the deletion of self-reactive T cells is incomplete, thymic development

230 affinity in modulating the pathogenicity of self-reactive T cells is less established.

231 Because self-reactive T cells may have low affinity for peptide:

232 Self-reactive T cells must escape thymic negative select

233 xist largely as distinct pathways to repress self-reactive T cells remains incompletely understood.

234 However, the molecular identity of these self-reactive T cells remains largely elusive.

235 lerance plays a critical role in eliminating self-reactive T cells specific for peripheral antigens.

236 Self-reactive T cells that escape elimination in the thy

237 Foxp3 is expressed in a fraction of self-reactive T cells that escape negative selection in

238 s exist to prevent autoimmune destruction by self-reactive T cells that escape thymic deletion.

239 Tregs are critical for control of self-reactive T cells that escape thymic selection and e

240 ncluding multiple sclerosis, are mediated by self-reactive T cells that have escaped the deletional m

241 quiescent tissue-resident dendritic cells to self-reactive T cells that have escaped thymic negative

242 which regulates immune tolerance) that allow self-reactive T cells to enter the periphery.

243 Such compensatory mechanisms can allow self-reactive T cells with altered TCR-binding propertie

244 In T cell-mediated autoimmune diseases, self-reactive T cells with known antigen specificity app

245 Whereas thymic education eliminates most self-reactive T cells, additional mechanisms to promote

246 lammatory disease, spontaneous activation of self-reactive T cells, and autoantibody production are h

247 Microbial peptides can activate self-reactive T cells, but the structural basis for such

248 ion of apoptosis resulted in more persistent self-reactive T cells, but these cells became anergic to

249 sing the transcription factor Foxp3 suppress self-reactive T cells, prevent autoimmunity, and help co

250 These peptidic arrays are used to purge self-reactive T cells, thereby averting autoimmunity.

251 ntation and epitope-dependent elimination of self-reactive T cells, which may explain why the fat10 g

252 Further, TCRs found on potentially self-reactive T cells, with an activated phenotype (CD4+

253 akdown of tolerance mechanism and priming of self-reactive T cells.

254 immune responses and autoimmunity caused by self-reactive T cells.

255 lity to modulate the activation threshold of self-reactive T cells.

256 hymic expression of self-Ags and deletion of self-reactive T cells.

257 s from the mechanisms that usually eliminate self-reactive T cells.

258 echanism underlying the anergic phenotype of self-reactive T cells.

259 l tolerance by suppressing the activation of self-reactive T cells.

260 T cells, substantiating the presence of such self-reactive T cells.

261 thogens and inducing peripheral tolerance in self-reactive T cells.

262 egy for purging the peripheral repertoire of self-reactive T cells.

263 immune pathways but is primarily mediated by self-reactive T cells.

264 reby allowing us to characterize the exposed self-reactive T cells.

265 he recognition of multiple GAD65 peptides by self-reactive T cells.

266 In this way, self-reactive T lymphocytes that would attack peripheral

267 Although self-reactive T-cell precursors can be eliminated upon r

268 SG to CD1c enables the binding of human CD1c self-reactive T-cell receptors.

269 that provide a footprint for binding of CD1c self-reactive T-cell receptors.

270 These data show how binding by a self-reactive TCR favors crossreactivity between self an

271 ugh the expression of a newly generated, non-self-reactive TCR.

272 Two broad categories of self-reactive TCRs can be clearly distinguished: (i) TCR

273 an permit the survival of T cells expressing self-reactive TCRs that nonetheless bind with a traditio

274 ing that there are multiple unusual ways for self-reactive TCRs to bind their pMHC ligand.

275 cells pose an autoimmune hazard by allowing self-reactive TCRs to escape thymic selection.

276 x are distinct from previously characterized self-reactive TCRs, indicating that there are multiple u

277 apeutic TCR surface expression and generates self-reactive TCRs.

278 DR3beta robustly promoted the development of self-reactive TCRs.

279 Once induced, the self-reactive TH17 cells promoted auto-inflammation and

280 ion, presumably through the amplification of self-reactive Th17 cells.

281 However, the mechanism by which self-reactive thymocytes are diverted into the Treg cell

282 In the thymus, high-affinity, self-reactive thymocytes are eliminated from the pool of

283 However, many self-reactive thymocytes first encounter ubiquitous self

284 utoimmunity by limiting agonist selection of self-reactive thymocytes into the Treg cell lineage.

285 Thus, we propose that the selection of self-reactive thymocytes into the Treg cell subset occur

286 Negative selection against highly self-reactive thymocytes is critical for preventing auto

287 icity as a primary determinant for selecting self-reactive thymocytes to become Treg cells in a multi

288 rimarily mediated through clonal deletion of self-reactive thymocytes, is critical for establishing s

289 m is not required for the clonal deletion of self-reactive thymocytes, suggesting the existence of no

290 Aire results in impaired clonal deletion of self-reactive thymocytes, which escape into the peripher

291 peripheral-tissue antigens (PTAs) to delete self-reactive thymocytes.

292 tissue Ags, and promotes clonal deletion of self-reactive thymocytes.

293 estricted Ags that induce clonal deletion of self-reactive thymocytes.

294 TSAs), which are presented and help tolerize self-reactive thymocytes.

295 r B cell tolerance via positive selection of self-reactive transitional B cells.

296 quency of these cells are similar to that of self-reactive Tregs in the absence of cognate infection.

297 which TCR affinity regulates the function of self-reactive Tregs is largely unknown.

298 lusion of cells expressing the intrinsically self-reactive V(H)81X from both pools.

299 Hence, B cells expressing germline-encoded self-reactive VH4-34 antibodies may represent an innate-

300 ecludes secondary rearrangements that delete self-reactive VJ rearranged genes.