ライフサイエンスコーパス: immature B-cell

1 sential for a pre-B cell to traverse into an immature B cell.

2 from large pre-B cells to small B cells and immature B cells.

3 e cell line WEHI-231 have been classified as immature B cells.

4 major source of autoantibodies compared with immature B cells.

5 unappreciated role for Bright regulation in immature B cells.

6 nvolved in receptor editing of self-reactive immature B cells.

7 eage EU12 cell line and in human bone marrow immature B cells.

8 a successful transition from pre-B cells to immature B cells.

9 om microMT mice, but undetectable in pre- or immature B cells.

10 lation occurred mainly with naive mature and immature B cells.

11 editing in autoreactive and non-autoreactive immature B cells.

12 on, and rapid turnover, had the phenotype of immature B cells.

13 e cell line WEHI-231 have been classified as immature B cells.

14 to different pathways of death signaling in immature B cells.

15 le-stranded DNA breaks at V(H) cRSS sites in immature B cells.

16 ic genes A1 and bcl-x(L) in MB cells but not immature B cells.

17 cells and was extinguished in large preB and immature B cells.

18 mally expressed only in B cell precursors or immature B cells.

19 sic signaling differences between mature and immature B cells.

20 se opposing outcomes are signaled by BCRs on immature B cells.

21 ce in the outcome of signaling in mature and immature B cells.

22 expressing B cells in unimmunized spleen are immature B cells.

23 nd apoptosis, receptor editing, or anergy in immature B cells.

24 milar signaling pathways in human and murine immature B cells.

25 pression in a discrete subset of bone marrow immature B cells.

26 is responsible for the apoptotic response of immature B cells.

27 of B7 molecules leads to the elimination of immature B cells.

28 ), is selectively expressed by the pre-B and immature B cells.

29 cells, cycling pre-B cells, and IgM+, IgD-/+ immature B cells.

30 ort half-lives equivalent to those of non-Tg immature B cells.

31 oglobulin light chain gene rearrangements in immature B cells.

32 ivate an overlapping set of kinases in human immature B cells.

33 hibits growth and induces apoptosis in human immature B cells.

34 ocking B cell receptor-mediated apoptosis in immature B cells.

35 xplored the effects of TGF beta1 on WEHI 231 immature B cells.

36 cell cycle progression and proliferation of immature B cells.

37 s thymic enlargement and excessive export of immature B cells.

38 f CD1d expression exclusively in repopulated immature B cells.

39 ition impaired the differentiation of normal immature B cells.

40 -coupled genotoxic activity in self-reactive immature B cells.

41 ling, respectively, the numbers of pre-B and immature B cells.

42 ent of the B Cell Receptor (BCR) of WEHI 231 immature B cells, a drop in c-Myc expression is followed

43 population that regulated fate decisions by immature B cells after Ag receptor signaling.

44 cell tolerance by promoting the survival of immature B cells after engagement of the B cell antigen

45 Rag expression can continue in immature B cells, allowing continued Igkappa V(D)J recom

46 levels of active Erk and Ras in autoreactive immature B cells, although this is evident only when the

47 of the kappa locus is biallelic in wild-type immature B cells and in recombination activating gene (R

48 TSLP) supports the development of B220+ IgM+ immature B cells and induces thymocyte proliferation in

49 and Erk in nonautoreactive and autoreactive immature B cells and investigated whether activation of

50 at somatic hypermutation can occur in murine immature B cells and may represent a mechanism for enlar

51 excluding the influence of splenic influx of immature B cells and passive acquisition of FcgammaRIIB

52 reased Ag-induced mobilization of calcium in immature B cells and presumably ensure elimination of au

53 nd suggest an ontological connection between immature B cells and regulatory plasmablasts.

54 vels on nonautoreactive than on autoreactive immature B cells and that its expression correlates with

55 in, and phospholipase Cgamma2 is enhanced in immature B cells and they exhibit greater capacitative c

56 letion of splenic natural killer (NK) cells, immature B cells, and B progenitor cells in bone marrow

57 ature T cells parallels that which occurs in immature B cells, and has important implications for und

58 h little in pro-B cells, moderate amounts in immature B cells, and high levels selectively in mature

59 was low in progenitor B cells, increased in immature B cells, and highest in mature B cells.

60 deletion and receptor-editing mechanisms in immature B cells, and may suggest a higher affinity thre

61 e-B cells, decreased as cells developed into immature B cells, and then increased again upon transiti

62 kout (B-S1pr1KO) mice, their newly generated immature B cells appeared in the blood at abnormally low

63 shown that in certain cases, progenitor and immature B cells are capable of editing their receptors

64 hat anergic as well as acutely Ag-stimulated immature B cells are defective in stromal cell-derived f

65 ansgenic system, we show that IgM(high) late-immature B cells are fully capable of receptor editing t

66 Because most immature B cells are lost at this transition, this putat

67 Our experiments reveal that when immature B cells are near BM sinusoids their motility is

68 the numbers of progenitor pro-B, pre-B, and immature B cells are reduced by 30-40% in B cell-specifi

69 s a dominant mechanism by which autoreactive immature B cells are rendered tolerant.

70 Newly generated immature B cells are selected to enter the peripheral ma

71 ced responses are developmentally regulated; immature B cells are tolerized following antigenic expos

72 nals to B cell receptor-engaged transitional immature B cells argues that these B cells may be direct

73 To determine where in the cell cycle immature B cells arrest, we have examined the expression

74 chains generates IgM, which is expressed on immature B cells as the B-cell antigen-binding receptor

75 In contrast to wild-type immature B cells, B cell receptor engagement of PTEN-def

76 Our findings indicate that in immature B cells, basal activation of Ras and Erk are co

77 ntibodies and is consistent with the loss of immature B cells bearing 2F5 chimeric antibodies to cent

78 Previous studies have suggested that late immature B cells, bearing high levels of IgM on their ce

79 thway rescued the differentiation of BCR-low immature B cells both in vitro and in vivo, whereas extr

80 ments in at least two-thirds of autoreactive immature B cells, but fails to accelerate cell death at

81 tor-editing signals are given to bone marrow immature B cells by antiidiotype antibody or after in vi

82 be important for efficient transformation of immature B cells by the v-abl oncogene.

83 Moreover, immature B cells carrying an innocuous receptor have sus

84 In immature B cells carrying innocuous receptors, RAG expre

85 population, increased numbers of circulating immature B cells, CD19+,IgD+,CD38(high),CD10(low),CD24(h

86 reassembled VL gene led not only to a larger immature B cell compartment but also to a decrease in "d

87 TM, which do not reach high levels until the immature B cell compartment, the stage at which receptor

88 old required for positive selection into the immature B cell compartment.

89 We propose that in the pre-B and immature B cell compartments, gradients of E12 and E47 a

90 Recent studies indicate that immature B cells compete with recirculating B cells for

91 ther, these data clearly demonstrate that T2 immature B cells comprise a discrete developmental subse

92 small increase in egr-1 expression in normal immature B cells consistent with their inability to prol

93 the mechanisms whereby antigen receptors on immature B cells deliver inhibitory signals (leading to

94 nt contraction by looping in small pre-B and immature B cells, demonstrating that immunoglobulin loci

95 pensated by increased proliferation in adult immature B cells, despite increased Ki67 expression.

96 haracterized; the process that governs which immature B cells develop into long-lived peripheral B ce

97 Immature B cells developing in the bone marrow are found

98 e thymic stromal lymphopoietin (TSLP) drives immature B cell development in vitro and may regulate T

99 esponsible for this activity nor its role in immature B cell development in vivo were addressed by th

100 several loci required for the pre-B cell to immature B-cell developmental transition.

101 Unlike the immature B lymphoma cells, normal immature B cells did not exhibit constitutive MAPK activ

102 iggered responses of mature and transitional immature B cells differ at both the biochemical and func

103 Immature B cells display greater increases in intracellu

104 Immature B cells display increased sensitivity to tolera

105 to 75%) of all antibodies expressed by early immature B cells displayed self-reactivity, including po

106 lowing BCR aggregation, whereas transitional immature B cells do not.

107 bal "back-differentiation" response in which immature B cells down-regulate genes important for the m

108 al genome in bone marrow pro-pre-B cells and immature B cells during early latency and immature B cel

109 nd immature B cells during early latency and immature B cells during long-term latency.

110 Immature B cell egress from BM was dependent on a twofol

111 We recently reported that an immature B cell encounter with cognate self-Ag in the bo

112 Using two-photon microscopy, we found immature B cells entering and crawling in sinusoids; the

113 reverted most BM alterations, but ERT led to immature B-cell expansion.

114 Immature B cells express constitutive nuclear factor-kap

115 n/mouse Igmu chain but not the production of immature B cells expressing membrane IgM.

116 evel of cell surface CD19, and appearance of immature B cells expressing mu/kappa or mu/lambda cell s

117 ial chromosome reporter as well as wild-type immature B cells following Ag incubation.

118 n of mature B cells and during the rescue of immature B cells from apoptosis.

119 e demonstrate that PKC activation can rescue immature B cells from BCR-induced apoptosis.

120 )3 and V(H)4 family repertoires of pre-B and immature B cells from bone marrow and mature B cells fro

121 ccumulation, trigger premature emigration of immature B cells from bone marrow.

122 02, two potent inhibitors of Pl 3-K, rescued immature B cells from CD38-mediated growth suppression.

123 n, a p70 S6-kinase inhibitor, did not rescue immature B cells from CD38-mediated suppression.

124 the Ly108 gene was most highly expressed in immature B cells from lupus-prone B6.Sle1z mice.

125 Immature B cells from normal mouse bone marrow were not

126 rtantly, cross-linking sIgD does not protect immature B cells from sIgM-induced apoptosis.

127 or the efficient transfer of newly generated immature B cells from the bone marrow to the blood.

128 Supporting this hypothesis, we found that immature B cells from xid (x-linked immunodeficiency) mi

129 itor in B cells would rescue mature, but not immature, B cells from tolerance induction.

130 Thus, the abundance of immature B cells generated in Vav-null mice may be due t

131 CR ligation of WEHI 231 as well as of normal immature B cells greatly increased expression of CTCF in

132 k of IL-7 in the survival of pro-, pre-, and immature B cells; however, lack of Bim did not substitut

133 ely low level of cholesterol in transitional immature B cells impairs compartmentalization of their B

134 Notably, immature B cells in aged bone marrow exhibit a similar p

135 Endogenous RAG messenger RNA is expressed in immature B cells in bone marrow and spleen and decreases

136 0(+)IgM(-) pro/pre-B cells and B220(+)IgM(+) immature B cells in bone marrow.

137 In the bone marrow of B-S1pr1KO mice, immature B cells in contact with the vascular compartmen

138 y low-dose self-antigen promotes survival of immature B cells in culture.

139 Thus, activation of immature B cells in GALT may function as a checkpoint th

140 TdT expression suggests the presence of immature B cells in RA synovia.

141 We observe that immature B cells in SLE are poorly equipped to access th

142 We find a dominant population of immature B cells in the blood and spleen early, followed

143 ne marrow B cells also reduced the number of immature B cells in the blood.

144 e find that the reporter is expressed in all immature B cells in the bone marrow and spleen.

145 in the immune system suggest that only those immature B cells in the bone marrow that undergo recepto

146 induced abnormal apoptosis of premature and immature B cells in the bone marrow, and led to peripher

147 ely required for survival and progression of immature B cells in the bone marrow, they nevertheless m

148 he mature IgM+ B population but not from the immature B cells in the bone marrow.

149 contribution of NF-kappaB to the survival of immature B cells in the bone marrow.

150 atively, from accumulation of RAG-expressing immature B cells in the periphery.

151 ulting in the accumulation of RAG-expressing immature B cells in the spleen.

152 oincides with accumulation of RAG-expressing immature B cells in the spleen.

153 that can be found in close association with immature B cells in vivo.

154 e in the number and frequency of bone marrow immature B cells in vivo.

155 s, particularly CD43(low/-)B220(+) pre-B and immature B cells, in influenza virus-infected mice.

156 ane type II glycoprotein highly expressed in immature B cells, inhibits cell growth and causes apopto

157 ping B cells in bone marrow, did not release immature B cells into the blood of B-S1pr1KO mice as eff

158 c mice given doxycycline showed an influx of immature B cells into the periphery, with population exp

159 o aid the differentiation of nonautoreactive immature B cells into transitional B cells and to promot

160 differentiation of CD19(+)CD24(hi)CD38(hi) (immature) B cells into IL-10-producing CD24(+)CD38(hi) B

161 is in fact selective, in that the fate of an immature B cell is highly dependent on its Ig receptor s

162 It therefore appears that when the BCR of an immature B cell is ligated, PIP3 levels are reduced, PLC

163 s a consequence, the pool of new bone marrow immature B cells is markedly reduced in size and clonal

164 Basal activation of Erk in immature B cells is proportional to surface IgM and depe

165 emonstrating that the expression of IRF-4 in immature B cells is rapidly induced by self-antigen and

166 However, most AID+ immature B cells lacked anti-apoptotic MCL-1 and were de

167 ngagement of the B cell receptor of WEHI 231 immature B cells leads sequentially to a drop in c-Myc,

168 iated with surrogate light chain and the 1E8 immature B cell line expressing cell surface mu/kappa.

169 When RelA was overexpressed in the immature B cell line WEHI 231 or the mature B cell line

170 s of mitogen-activated protein kinase in the immature B cell line WEHI-231, in immature splenic B cel

171 o prevent anti-IgM-induced cell death of the immature B cell line WEHI-231.

172 In this report the mouse immature B cell line, WEHI 231, was used to examine the

173 Here we show that the BCR in the immature B cell line, WEHI-231, does not translocate int

174 stitutive NF-kappaB activity in the WEHI-231 immature B cell line.

175 e demonstrate that K13 protects WEHI 231, an immature B-cell line, against anti-IgM-induced growth ar

176 Treatment of the more immature B-cell line, Ramos, with phorbol esters rescues

177 R-induced growth arrest and apoptosis in the immature B-cell line, WEHI-231.

178 ine their ability to induce apoptosis in the immature B-cell line, WEHI-231.

179 Unstimulated immature B cell lines (WEHI-231 and CH31) and unstimulat

180 Short-term culture of immature B cell lines in the presence of apoptogenic sti

181 In the B cell receptor-negative immature B cell lines RS4;11, 380, and REH, Ig alpha and

182 In contrast, BCR-stimulated immature B cell lines undergo growth arrest and coincide

183 nt study, we found that CD38 ligation in the immature B-cell lines 380, REH, and RS4;11 caused rapid

184 gation of B cell receptor (BCR) on BKS-2, an immature B cell lymphoma by anti-IgM antibodies (Ab) cau

185 Apoptosis of the WEHI 231 immature B cell lymphoma line following membrane interac

186 Stimulation of the phenotypically immature B cell lymphoma WEHI-231 with anti-IgM induces

187 loid, and T cells, physiologic cell death of immature B cell lymphomas correlated with a drop in c-my

188 cument that tolerance-sensitive transitional immature B cells maintain significantly lower membrane u

189 onto 125Tg mice reveals that, in contrast to immature B cells, mature anti-insulin B cells are exquis

190 data suggest that during an immune response, immature B cells may be able to sustain the responses of

191 of inositol-1,4,5-triphosphate production in immature B cells may be explained by enhanced inositol-1

192 3 wk of age, reflecting a lack of successful immature B cell migration to the periphery.

193 xpression, which leads to apoptosis in these immature B cell models of clonal deletion.

194 n addition, when mice are treated with flt3L immature B cells, natural killer (NK) cells and dendriti

195 Conversely, the bone marrow (BM) had reduced immature B cell numbers, but normal numbers of pro-B cel

196 vealed mild leukocytosis, including elevated immature B cell numbers.

197 marked (180% increase) hyperrepopulation of immature B cells occurred with conversion to mature B ce

198 In contrast, TdT was 3-fold upregulated in immature B cells of adults.

199 Most autoreactive cells exhibit an immature B cell phenotype and have short half-lives equi

200 g not only in bone marrow cells with a pre-B/immature B cell phenotype but also in immature/transitio

201 ests that removal of autoreactivity from the immature B cell pool also requires innate immunity pathw

202 tiple selection points within the peripheral immature B cell pool.

203 tal block at the T2-T3 transition within the immature B cell pool.

204 cts rescued B cell development and generated immature B cell populations in the bone marrow with simi

205 However, Ly-6I is also expressed on immature B cell populations that do not express Ly-6C.

206 ction between the bone marrow and peripheral immature B cell populations.

207 oduction but severely reduced proB/preB- and immature B-cell populations, indicating that Cdc42 is al

208 ent at approximately 3-fold higher levels in immature B cells, potentially contributing to increased

209 flow cytometric IgE CSR assay, we show that immature B cells preferentially switch to IgE versus IgG

210 CD45-/- B cells accumulated, despite normal immature B-cell production.

211 selection of subclones differentiating into immature B-cell progenitors as a mechanism of disease pr

212 nctions to various mature B-cell subsets but immature B-cell progenitors endowed with suppressive pro

213 Whereas immature B-cell progenitors survive the relatively low l

214 ition of calcineurin also results in reduced immature B cell proliferation in a similar manner, sugge

215 tion of IRF-4 expression in the IRF-4 mutant immature B cells promotes secondary rearrangement.

216 U12 muHC(+) cells and in the newly emigrated immature B cells purified from peripheral blood of healt

217 If the B cell receptor (BCR) on an immature B cell recognizes self-antigen, it is down-regu

218 AID expression was found in developmentally immature B cells recovered from murine fetal liver and f

219 nduction of biologically relevant responses: immature B cells require lower Ag concentrations for act

220 ty to negative selection, characterizing the immature B-cell response to B-cell antigen receptor (BCR

221 Importantly, induction of immature B cell responses requires much smaller increase

222 B cell receptor engagement of PTEN-deficient immature B cells resulted in activation and proliferatio

223 Igbeta deletion from large preB cells and immature B cells resulted in cell death that could be re

224 Rac1 activation is impaired in transitional immature B cells, resulting in defects in actin polymeri

225 wo-photon intravital microscopy to show that immature B cell retention within bone marrow (BM) was st

226 e is disrupted by PTPN22-R620W action during immature B cell selection, and PTPN22-R620W alters matur

227 on exposure to insulin, anti-insulin (125Tg) immature B cells show similar hallmarks of anergy as tho

228 cell signaling was greatly enhanced, whereas immature B cell signaling was minimally affected.

229 ls but does not effectively deplete pre-B or immature B cells, some B cell subpopulations, antibody-p

230 lates secondary Ig gene rearrangement at the immature B cell stage and contributes to cell fate deter

231 s required for B cell development beyond the immature B cell stage and that Ig alpha and Ig beta have

232 are members of the natural repertoire at the immature B cell stage is sufficient to promote editing.

233 umbers of autoreactive cells at the emergent immature B cell stage, and a relaxed selection for perip

234 shown that BAFFR is already expressed at the immature B cell stage, and that the prosurvival protein

235 ntional B cell development is blocked at the immature B cell stage, produce diverse H chain-only anti

236 ent of B2 cells was impaired at the pre- and immature B cell stage, resulting in decreased numbers of

237 on of miR-150 is sharply up-regulated at the immature B cell stage.

238 enforce the developmental checkpoint at the immature B cell stage.

239 uble Ags, extends through the IgM(high) late immature B cell stage.

240 y promotes B lymphopoiesis to the B220+/IgM+ immature B cell stage.

241 lambda V gene segment-cleavage events at the immature B cell stage.

242 reby antigen encounter at the Rag-expressing immature B-cell stage helps shape pre-immune BCR reperto

243 that promotes secondary rearrangement at the immature B-cell stage.

244 and Rag2 was repressed at the pro-B cell and immature B cell stages by the kinase Akt through its 'an

245 B cell differentiation beyond the pre-B and immature B cell stages, but it is unclear whether additi

246 eptor (pre-BCR) and the BCR at the pre-B and immature B cell stages, respectively.

247 Our results demonstrated that immature B cells stimulated with a low concentration of

248 nsion and skewing (lower T1/T2-ratio) of the immature B cell subset was noted in MC patients, suggest

249 which inhibit the growth arrest response of immature B cells, suppressed cyclin G2 mRNA expression i

250 es, the antigen receptor is expressed on the immature B cell surface and tested for autoreactivity le

251 ssion is essential to maintain preB cell and immature B cell survival and to mediate B cell different

252 B cells, but the role of Igmu expression in immature B cell survival has not been determined.

253 ains limited to a single D(H) produced fewer immature B cells than wild type.

254 higher percentage of pre-B2 cells but fewer immature B-cells than wild-type mice.

255 Immature B cells that encounter self-antigen are elimina

256 t the TR checkpoint, such that virtually all immature B cells that exit the bone marrow mature withou

257 es were produced in a discrete population of immature B cells that expressed recombination-activating

258 t studies indicate that these cells might be immature B cells that have not yet extinguished RAG expr

259 opment throughout life in the bone marrow to immature B cells that migrate to secondary lymphoid tiss

260 in early B cell development and they produce immature B cells that respond normally to BCR cross-link

261 since a UPR is also induced in transitional immature B cells that respond to BCR stimulation with a

262 In contrast, immature B cells that undergo BCR-induced apoptosis incr

263 expression restricted to a subpopulation of immature B cells, the B4B gene product may be involved i

264 rminal centers (GC) and decreased numbers of immature B cells; the genes targeted by OcaB were not de

265 ery, the absence of these signals allows the immature B cell to default to apoptosis as a result of B

266 s, reducing the absolute number of pre-B and immature B cells to 21% and 12% of normal, respectively,

267 Furthermore, the susceptibility of immature B cells to BCR-induced apoptosis is recapitulat

268 PKC may play a role in the susceptibility of immature B cells to BCR-induced apoptosis.

269 hat there is selection of only a minority of immature B cells to become mature B cells.

270 iated Ly108.1 allele, was found to sensitize immature B cells to deletion and RAG reexpression.

271 signals cooperate to enable nonautoreactive immature B cells to differentiate into transitional B ce

272 that the developmental window available for immature B cells to edit their Ig receptors, at least in

273 The failure of the BCR in immature B cells to enter lipid rafts may contribute to

274 ced by low-dose self-antigen, directed naive immature B cells to mature, not into the default follicu

275 E12 and E47 play critical roles in pre-B and immature B cells to promote immunoglobulin lambda (Ig la

276 l Ag receptor -induced apoptotic response of immature B cells toward continued recombination-activati

277 c exclusion that occurs at the pre-B cell to immature B cell transition and is dependent upon the IgH

278 's effect on IgH levels at the pre-B cell to immature B cell transition strongly influences allelic e

279 allelic exclusion took place at the pre-B to immature B cell transition.

280 -bound self-antigen, MRL/lpr 3-83 transgenic immature B cells undergo less endogenous rearrangement a

281 y exclusive biologic responses in mature and immature B cells: upregulation of CD86, CD69, and MHC cl

282 a(i) protein-coupled receptor upregulated in immature B cells, was required for sinusoidal retention.

283 this B cell population resembled bone marrow immature B cells, we examined the emigration of newly fo

284 markers characteristic of human bone marrow immature B cells, we have identified a population of cir

285 In this study we found that immature B cells were altered in frequency in the bone m

286 ls entering and crawling in sinusoids; these immature B cells were displaced by CB2 antagonism.

287 culture stage was used to determine if these immature B cells were functionally competent.

288 In bone marrow, immature B cells were normal in number, but internalized

289 ogenitors-from pre-pro-/early pro-B cells to immature B cells-were dramatically reduced and their pro

290 SLP)) promotes the development of B220+/IgM+ immature B cells when added to fetal liver cultures, lon

291 tolerance checkpoint is at the stage of the immature B cell, where receptor editing is the primary m

292 IgM is made selectively in immature B cells, whereas IgD is coexpressed with IgM wh

293 developmental arrest and receptor editing in immature B cells, whereas mature B cells have shortened

294 regulated by BCR-mediated signaling in human immature B cells, which can be modulated by physiologica

295 V)Socs3(fl/fl) mice had a 2-fold increase in immature B cells, which were evenly distributed in endos

296 for the negative selection of self-reactive immature B cells while simultaneously allowing for clona

297 Treatment of WEHI 231 immature B cells with an Ab against the surface IgM prot

298 autoantibody transgenic mice, reactivity of immature B cells with autoantigen can induce receptor ed

299 Incubation of immature B cells with self-Ag leads to a striking revers

300 In this study, immature B cells within the bone marrow of wild-type mic