ライフサイエンスコーパス: clonal deletion

1 or the beta-chain, which hinders rescue from clonal deletion.

2 le dose was insufficient to achieve complete clonal deletion.

3 cross-react with self-peptides resulting in clonal deletion.

4 H-induced apoptosis with that induced during clonal deletion.

5 leading to Ag-specific T cell activation and clonal deletion.

6 echanisms of tolerance: receptor editing and clonal deletion.

7 l surface) to create an agent for CD8 T-cell clonal deletion.

8 al clonal exhaustion, followed by peripheral clonal deletion.

9 hese self-antigens within the thymus undergo clonal deletion.

10 responses involves both anergy induction and clonal deletion.

11 because all of these elements contribute to clonal deletion.

12 ay of self-peptides resulting in inefficient clonal deletion.

13 is attained by receptor editing, anergy, or clonal deletion.

14 orted roles in tissue-restricted Ag-mediated clonal deletion.

15 l superantigen induced a clan III-restricted clonal deletion.

16 that P1A-specific T cells are susceptible to clonal deletion.

17 ure CD4+CD8+ (DP) thymocytes, referred to as clonal deletion.

18 o autoreactivity in the periphery results in clonal deletion.

19 apoptosis in these immature B cell models of clonal deletion.

20 fic transplant tolerance analogous to thymic clonal deletion.

21 s developed, at least in part, by intragraft clonal deletion.

22 ved are, instead, attributable to effects of clonal deletion.

23 es was not solely due to reported defects in clonal deletion.

24 ation of T cells that would normally undergo clonal deletion.

25 +)Foxp3(+) Treg development without inducing clonal deletion.

26 cell autoreactivity in the absence of thymic clonal deletion.

27 lear quantitative defects in antigen-induced clonal deletion.

28 l tolerance enforced by receptor editing and clonal deletion.

29 ambda, in pAlb mice, kappa B cells underwent clonal deletion.

30 is largely unknown how these T cells escape clonal deletion.

31 w, via a combination of receptor editing and clonal deletion.

32 ood about the molecular mechanism leading to clonal deletion.

33 ork for understanding the molecular basis of clonal deletion.

34 th a conalbumin-specific TCR prone to thymic clonal deletion acquired peptide-specific T cell respons

35 p24 Ag in HIV-infected individuals and that clonal deletion alone does not explain this phenomenon.

36 Clonal deletion analysis of OPN promoter-luciferase cons

37 s was associated with peripheral and central clonal deletion and a higher frequency of regulatory T c

38 Whereas clonal deletion and anergy are mechanisms of peripheral

39 ms of B cell tolerance are receptor editing, clonal deletion and anergy.

40 ve B lymphocytes that escape inactivation or clonal deletion and are examples of "clonal ignorance."

41 d in many ways, does not require a thymus or clonal deletion and can spread to third-party antigens l

42 antigen-specific systemic tolerance by both clonal deletion and clonal anergy.

43 ed by large naive populations induce minimal clonal deletion and contain certain amino acids with the

44 , 2) unable to secrete Ab, 3) able to escape clonal deletion and develop into B1 B cells in the perit

45 signals results in outcomes as divergent as clonal deletion and differentiation to the unconventiona

46 1H3.1 alphabeta TCR Tg T cells have escaped clonal deletion and efficiently populated the periphery.

47 trating OT-I CD8(+) T cells that had escaped clonal deletion and gained effector functions before dev

48 Bim and Nur77 during ubiquitous Ag-mediated clonal deletion and highlight potential differences from

49 CD28KO pregnants in contrast to the partial clonal deletion and hyporesponsiveness of remaining T ce

50 CD28 as the intrathymic signal required for clonal deletion and identifies CD8alphaalpha(+) IELs as

51 th limited thymic expression induced partial clonal deletion and impaired effector T cell potential b

52 apoptosis pathway from that activated during clonal deletion and indicate that signaling cascades lea

53 fficient T cell apoptosis may interfere with clonal deletion and maintenance of tolerance, and result

54 mbles the signaling cascade activated during clonal deletion and modeled by B cell receptor cross-lin

55 article, I trace the historic background of clonal deletion and molecular mimicry, two major pillars

56 However, the relative contributions of clonal deletion and receptor editing to B cell tolerance

57 to be maintained at least partially through clonal deletion and suppression.

58 ion of antigen-specific T cells, followed by clonal deletion and survival of a small number of memory

59 sion activates apoptosis of B cell models of clonal deletion and that rescue from apoptosis by CD40 l

60 endent processes are thought to promote both clonal deletion and the development of Foxp3(+) regulato

61 raft survival correlated with donor-specific clonal deletion and the presence of donor class II mRNA

62 ays an important role in normal processes of clonal deletion and they indicate that the NF-kappaB/Ika

63 expression of nuclear hLa Ag induces thymic clonal deletion and tTreg selection, and lymphocytic inf

64 e spleens of mixed chimeras, suggesting that clonal deletion and/or receptor editing may maintain B-c

65 aintain B-cell tolerance to Gal, probably by clonal deletion and/or receptor editing.

66 th production of donor T-cells and effective clonal deletion, and a significant reduction in activate

67 Receptor editing, clonal deletion, and anergy are the mechanisms by which

68 undergo tolerance, such as receptor editing, clonal deletion, and anergy, have been established in mi

69 luding editing of the B cell receptor (BCR), clonal deletion, and anergy.

70 and B7-2 and their receptor CD28 can promote clonal deletion, and limited in vivo studies have indica

71 Multilineage chimerism, clonal deletion, and lymphocyte subsets were analyzed by

72 at in mixed allogeneic chimeras, intrathymic clonal deletion, and not peripheral suppression or anerg

73 ious mechanisms, including receptor editing, clonal deletion, and receptor downregulation.

74 fector function and proliferative potential, clonal deletion, and significantly decreased occurrence

75 olerance to bone marrow transplants involves clonal deletion, and tolerance to heart allografts in th

76 iety of self-tolerance mechanisms, including clonal deletion, anergy, and clonal ignorance.

77 that autoreactive B cells are controlled by clonal deletion, anergy, and developmental arrest.

78 nt functional CTL responses, arguing against clonal deletion as a mechanism for the decline of CTL re

79 ath of T cells is consistent with peripheral clonal deletion as one mechanism of tolerance.

80 one marrow has recently been associated with clonal deletion, as reported in fully allogeneic models

81 pendent endogenous loading was essential for clonal deletion at limiting antigen doses.

82 homa is used as a model of self-tolerance by clonal deletion because B cell receptor (BCR) ligation r

83 one of the principal mediators implicated in clonal deletion, Bim, is required for caspase-3 activati

84 ative selection of crossreactive TCRs led to clonal deletion but also recycling into intestinal CD4(-

85 the chromosome 3 (Chr3) regions that control clonal deletion, but mainly to two regions on Chr1 and C

86 nding in T cells leads to inefficient thymic clonal deletion, but T cell tolerance is maintained by F

87 eptors (TCR) can adopt differing cell fates: clonal deletion by apoptosis or deviation into alternati

88 cells, BM-derived cells extend the range of clonal deletion by cross-presenting antigen captured fro

89 ve thymocytes were prevented from undergoing clonal deletion by either a lack of CD28 costimulation o

90 a B cell tolerance mechanism in addition to clonal deletion, clonal anergy, and receptor editing.

91 her molecule thought to be a key mediator of clonal deletion, could be responsible for Bim-independen

92 of P1A antigen in the thymus induces T cell clonal deletion demonstrates that normal hematopoietic c

93 olerance induction by impairing BCR-mediated clonal deletion, deregulating receptor editing, and decr

94 Therefore, clonal deletion does not appear to explain the induction

95 lls are positively selected in K14 mice, but clonal deletion does not ocur in K14 mice or in relB-neg

96 ence, P1A-specific T cells must have escaped clonal deletion due to low expression of P1A in the thym

97 , suggesting that autoreactive B cells elude clonal deletion during development.

98 We now report that clonal deletion during negative selection required CD28-

99 Autoreactive thymocytes can be eliminated by clonal deletion during their development in the thymus.

100 ombined deficiency in Bim and Nur77 impaired clonal deletion efficiency and significantly increased p

101 It has long been thought that clonal deletion efficiently removes almost all self-spec

102 sHEL in this model system in order to block clonal deletion fails to rescue survival of mature B cel

103 The latter mice naturally acquire clonal deletion for autoreactive OT-I CD8(+) T cells (pa

104 latory mechanisms in addition to intrathymic clonal deletion for the maintenance of tolerance to reci

105 reactivity in the B-cell compartment include clonal deletion, functional inactivation and receptor ed

106 populations, (2) the physiologic process of clonal deletion functions to remove clones that have rea

107 nce, but the intrathymic signals that induce clonal deletion have not been clearly identified.

108 und T-cell tolerance most likely mediated by clonal deletion, (ii) T-cell clonal ignorance, and (iii)

109 pression can be used as a specific marker of clonal deletion in an unmanipulated thymus and directly

110 t's lymphoma, is a model for antigen-induced clonal deletion in germinal center B-lymphocytes, with a

111 ell tolerance is maintained by Fas-dependent clonal deletion in LN and spleen.

112 y timed and a ubiquitous self-antigen drives clonal deletion in male mice.

113 However, the significance of B7-mediated clonal deletion in preventing autoimmune diseases has no

114 tion, Bim has been shown to be important for clonal deletion in several model systems, whereas Nur77

115 deletion nor did it exacerbate the defect in clonal deletion in the absence of Bim.

116 conventional alphabetaT cells are subject to clonal deletion in the medulla, entry into the thymus me

117 nd molecular nature of two distinct waves of clonal deletion in the normal thymus.

118 accepted that developing T cells can undergo clonal deletion in the thymus in response to a high affi

119 The self-reactive T cells that escape clonal deletion in the thymus must be suppressed by the

120 c for an unmutated tumor Ag can be shaped by clonal deletion in the thymus.

121 g cells) are largely autoreactive yet escape clonal deletion in the thymus.

122 8 absence did not impair TCR-V beta-specific clonal deletion induced by neonatal exposure to MMTV.

123 n has, however, remained controversial, with clonal deletion, induction of suppressor cells or of typ

124 Our data further suggest that clonal deletion is a default pathway that functions only

125 These results demonstrate that clonal deletion is a major mechanism for tolerance to Ag

126 Clonal deletion is arguably the most important mechanism

127 Thus, when clonal deletion is circumvented, kappa editing and anerg

128 In contrast, clonal deletion is mediated by dendritic cells and medul

129 Clonal deletion is necessarily T cell receptor (TCR) spe

130 (b) Clonal deletion is not the mechanism of underlying long-

131 To examine whether the T cell clonal deletion is responsible for the tolerance, we cro

132 ough there is evidence that they can support clonal deletion, it is not clear whether they do so dire

133 cells not controlled by receptor editing or clonal deletion may become anergic.

134 The critical role of B7-1 and B7-2 in T cell clonal deletion may explain, at least in part, the parad

135 self-reactive T cells by altering the thymic clonal deletion mechanism, or reduce the production of C

136 es, suggesting the existence of nonapoptotic clonal deletion mechanisms.

137 As in clonal deletion models, and as predicted by the down-reg

138 ur77 deficiency did not substantially impact clonal deletion nor did it exacerbate the defect in clon

139 etic (NOD) genetic variation impairs neither clonal deletion nor downstream transcriptional programs.

140 These data indicate that clonal deletion normally occurs at a relatively late sta

141 These data demonstrate that efficient clonal deletion occurs after partial myeloablation and t

142 The precise developmental stage(s) at which clonal deletion occurs in a normal thymus has been diffi

143 Such joins are not expected if clonal deletion occurs, because the progenitor cell woul

144 y a role in peripheral tolerance mediated by clonal deletion of Ag-specific T cells.

145 /II MHC-disparate cells despite early thymic clonal deletion of alloreactive cells.

146 nd degree of humoral tolerance was caused by clonal deletion of alloreactive specificities from the p

147 nce in experimental models, which implicates clonal deletion of alloreactive T and B cells, induction

148 We conclude that ESC may induce clonal deletion of alloreactive T cells by Fas-induced a

149 volves that is permanent and associated with clonal deletion of alloreactive T cells.

150 s receptor signaling is not the mechanism of clonal deletion of antigen-reactive cells after antibody

151 Clonal deletion of autoreactive B cells is crucial for t

152 reveal that costimulatory molecules enhance clonal deletion of autoreactive T cells as well as gener

153 Clonal deletion of autoreactive T cells in the thymus is

154 Clonal deletion of autoreactive thymocytes is important

155 ining 20-30 copies of the transgene, massive clonal deletion of B cells was observed in the bone marr

156 ted that a key obstacle to BnAb induction is clonal deletion of BnAb-expressing B cells.

157 Extensive thymic clonal deletion of CD4(+) T cells occurred in H-2(k/k) d

158 e fact that VIP and PACAP prevent Ag-induced clonal deletion of CD4+ T cells, but not that of CD8+ T

159 PTAs) in thymic stromal cells, promoting the clonal deletion of differentiating T cells that recogniz

160 but maintained to third-party antigens, and clonal deletion of donor-reactive host Vbeta T cells.

161 ipients, demonstrating a role for peripheral clonal deletion of donor-reactive T cells after allogene

162 Long-term mixed hematopoietic chimerism, clonal deletion of donor-reactive T cells, and bidirecti

163 dult thymectomized, ALS-treated mice induced clonal deletion of donor-reactive T cells.

164 followed by gradual, presumably peripheral, clonal deletion of donor-reactive T cells.

165 ct and indirect antigen presentation lead to clonal deletion of effector T cells in chimeras.

166 at bind specifically to foreign antigens and clonal deletion of equivalent B cells that bind self-ant

167 failed to abrogate the process of peripheral clonal deletion of H(+)/K(+) ATPase-specific CD4 T cells

168 We found that clonal deletion of highly autoreactive B cells in the bo

169 Clonal deletion of HIV-specific cytotoxic T-cell clones

170 men despite the development of chimerism and clonal deletion of host T cells to donor MHC-Ags in the

171 trathymic and extrathymic chimerism, and for clonal deletion of host-type thymocytes with TCR recogni

172 articipant in events leading to TCR-mediated clonal deletion of immature thymocytes.

173 Direct presentation for clonal deletion of MHC class II-restricted thymocytes re

174 Marked clonal deletion of mouse thymocytes bearing a transgenic

175 Therefore, miR-181a helps to guarantee the clonal deletion of particular moderate-affinity clones b

176 etition with mTg-derived peptides may impede clonal deletion of pathogenic, mTg-specific T cells in t

177 on, induction of HO-1 expression accelerates clonal deletion of peripheral alloreactive CD4+ T cells

178 Moreover, donor Ag-driven clonal deletion of recipient T cells occurred only in ch

179 Clonal deletion of self-reactive T cells was investigate

180 Deficient clonal deletion of self-reactive thymocytes was demonstr

181 gative selection, primarily mediated through clonal deletion of self-reactive thymocytes, is critical

182 -antigens (UbA), Bim is not required for the clonal deletion of self-reactive thymocytes, suggesting

183 The absence of Aire results in impaired clonal deletion of self-reactive thymocytes, which escap

184 riety of peripheral tissue Ags, and promotes clonal deletion of self-reactive thymocytes.

185 e array of tissue restricted Ags that induce clonal deletion of self-reactive thymocytes.

186 IEk bound to the MCC variant caused the clonal deletion of some T cells specific for the IEk + M

187 have indicated that CD28 is involved in the clonal deletion of some T cells.

188 of B7-1 and B7-2 substantially inhibits the clonal deletion of T cells in the thymus and leads to an

189 , and is most likely mediated by intrathymic clonal deletion of T cells that recognize antigens expre

190 erance induction, which is associated with a clonal deletion of T-cell subsets.

191 The rapid and profound clonal deletion of the Ag-specific, peripheral T cells m

192 ht be an important checkpoint leading to the clonal deletion of the majority of effector T cells, pos

193 duced apoptosis has been used as a model for clonal deletion of thymocytes or peripheral T cells.

194 thymus led us to investigate its role in the clonal deletion of thymocytes.

195 hat graft acceptance was not due to complete clonal deletion of xenoreactive cells.

196 n only one of five tolerant rats, suggesting clonal deletion or a dense anergic state.

197 lymphocyte reaction responses, showing that clonal deletion or anergy did not occur, but that graft

198 that tolerance was not secondary to general clonal deletion or anergy of donor-reactive T cells.

199 ction, suggesting that neither chimerism nor clonal deletion or anergy of recipient T cells to alloan

200 absence of inflammatory signals resulted in clonal deletion or anergy of the T cell, respectively.

201 (BCR) with an auto-antigen results in either clonal deletion or functional inactivation.

202 controlling both intrathymic and extrathymic clonal deletion or inactivation of T cells, this objecti

203 ce induced to these Ags, ranging from T cell clonal deletion or inactivation to clonal "ignorance" of

204 nresponsive state is specific and not due to clonal deletion or irreversible functional inactivation

205 onses; virus-specific T cells either undergo clonal deletion or lose their ability to display the ful

206 Thus, bystander suppression does not reflect clonal deletion or reduced clonal expansion of the bysta

207 Clonal deletion originated as a critical element of the

208 Finally, in contrast to clonal deletion, PAH-induced pro/pre-B cell death was no

209 tral hypothesis in immunology, which is that clonal deletion plays an important role in preventing au

210 Clonal deletion, previously regarded as the major mechan

211 ell but rather is likely more dependent upon clonal deletion processes.

212 eceived living-donor kidney transplants with clonal deletion protocol (total lymphoid irradiation or

213 We conclude that clonal deletion prunes but does not eliminate self-speci

214 ssue of Immunity, Yu et al. (2015) show that clonal deletion prunes the T cell repertoire but does no

215 hat, despite being dispensable for thymocyte clonal deletion, RasGRP1 is critical for agonist selecti

216 id not abolish tolerance, suggesting central clonal deletion rather than anergy as the likely toleran

217 at H + L transgenic B cells are regulated by clonal deletion, receptor editing via secondary rearrang

218 otoxin beta receptor (LTbetaRIg) interrupted clonal deletion, reduced the size of the primary cancer,

219 ment, allowing self-reactive cells to escape clonal deletion; reducing transgenic TCR-mediated positi

220 eted Ag-specific thymocytes, and this thymic clonal deletion required CCR9-mediated homing and was pr

221 on status of the stimulatory APC, peripheral clonal deletion requires persistent Ag and is not determ

222 Whereas clonal deletion results in the death of developing autor

223 that these mechanisms represent two distinct clonal deletion strategies that are differentially imple

224 hree orders of magnitude, to agonist-induced clonal deletion, such that their proportion increased, g

225 ctivity (mixed lymphocyte coculture assays), clonal deletion (T-cell receptor Vbeta11 assay), periphe

226 d that the smaller population underwent more clonal deletion than the larger population.

227 Thus, rather than clonal deletion, the observed change in immune reactivit

228 In spite of defective clonal deletion, the T cells expressing the Tg TCR were

229 If we did have complete clonal deletion, there would be major voids, the infamou

230 A predominant mechanism for this is clonal deletion; though receptor editing, anergy inducti

231 of thymic peripheral antigen expression and clonal deletion to self-tolerance is demonstrated in the

232 Unlike UbA, clonal deletion to tissue-restricted antigens (TRAs) req

233 We found that clonal deletion to TRA was completely abrogated in the a

234 To study the role of Bim in clonal deletion to TRA, we constructed bone marrow (BM)

235 downstream of the T-cell receptor (TCR) for clonal deletion to UbA versus TRA and highlight the prof

236 his family of DNA-binding proteins in thymic clonal deletion, transgenic (Tg) mice bearing a dominant

237 Despite this clonal deletion, URO-OVA/OT-I mice spontaneously develop

238 active lymphocytes to negative selection and clonal deletion via apoptosis.

239 s of oral tolerance, TGF-beta production and clonal deletion via apoptosis.

240 To test the hypothesis of clonal deletion vs anergy, CTL limiting dilution assays

241 Clonal deletion was detectable 30 days after tolerance i

242 T cell receptor-Vbeta5.(1/2) and TCR-Vbeta11 clonal deletion was detected in host T cells in chimeras

243 nt in PG490-88-treated mice, suggesting that clonal deletion was not responsible for the observed tol

244 Clonal deletion was observed in 2C and HY models even wh

245 Clonal deletion was observed unexpectedly in 6C5.H-2(bxq

246 relative utilization of receptor editing vs clonal deletion, we determined the frequency of in-frame

247 Rather, thymocytes undergoing clonal deletion were preferentially associated with rare

248 hy some conditions promote tolerance through clonal deletion whereas others promote anergy.

249 c antigen-presenting cells were tolerated by clonal deletion, whereas peptides excluded from the thym

250 fferentiation (positive selection) or death (clonal deletion), which is dictated in large part by the

251 in the number of developing 1B2+ thymocytes (clonal deletion), which occurred primarily at the CD4+ C

252 ly recognize fetal/placental antigen undergo clonal deletion without priming for cytotoxic effector f