ライフサイエンスコーパス: B-cell differentiation

1 lls rescues the defects of BCR signaling and B cell differentiation.

2 first exons of genes that normally regulate B cell differentiation.

3 f CD138 and Blimp-1, markers for plasma-like B cell differentiation.

4 5; ERK; PI3K/Akt, and potently promote human B cell differentiation.

5 in ALL as a novel mechanism interfering with B cell differentiation.

6 ed occupation of the MZ, a niche favoring MZ B cell differentiation.

7 y regulatory loci to transiently suppress GC B cell differentiation.

8 fined age-related reference ranges for human B cell differentiation.

9 developmental defects at multiple stages of B cell differentiation.

10 ) cells and/or directly influence follicular B cell differentiation.

11 nship between virus latency and the stage of B cell differentiation.

12 e checkpoints at the postmutational stage of B cell differentiation.

13 induction of EBF at the Pro-B cell stage of B cell differentiation.

14 ce, is markedly induced during adipocyte and B cell differentiation.

15 l progenitors for subsequent STAT5-dependent B cell differentiation.

16 ceptor (PPAR)gamma/RXRalpha pathway on human B cell differentiation.

17 mperative to identify mediators that control B cell differentiation.

18 ne expression was critical at many stages of B cell differentiation.

19 and acquires features associated with T-bet+ B cell differentiation.

20 erentiation rather than just follicular (FO) B cell differentiation.

21 atment and ATRA had similar effects on human B cell differentiation.

22 d its expression is tightly regulated during B cell differentiation.

23 hat BAFF can also play an inhibitory role in B cell differentiation.

24 transcription factors that are critical for B cell differentiation.

25 n essential component for understanding late B cell differentiation.

26 otes cell cycle progression and inhibits pre-B cell differentiation.

27 all plasma cells, and required for terminal B cell differentiation.

28 omologue of BCL6 that represses IL-2-induced B cell differentiation.

29 long-term, persistent changes that accompany B cell differentiation.

30 h locus are developmentally regulated during B cell differentiation.

31 d antigen recognition is thought to regulate B cell differentiation.

32 eration; and increase Bcl-6, an inhibitor of B cell differentiation.

33 y the contribution of BCR signal strength in B cell differentiation.

34 cells will contribute to an understanding of B cell differentiation.

35 ndent on synthesis of immunoglobulins during B cell differentiation.

36 dant manner are required for antigen-induced B cell differentiation.

37 ne expression patterns that accompany mature B cell differentiation.

38 that DO protein levels are modulated during B cell differentiation.

39 nism responsible for the impaired Fancc(-/-) B cell differentiation.

40 on to express molecules necessary for plasma B cell differentiation.

41 determines the direction of IL-21-dependent B cell differentiation.

42 Here we address the role of Fra-2 in B cell differentiation.

43 undergoing dynamic methylation during normal B cell differentiation.

44 ning, and loss of polarity components during B cell differentiation.

45 rrelated with a subsequent enhancement in MZ B cell differentiation.

46 of Ets1 play an important role in inhibiting B cell differentiation.

47 ce of MCs negatively affects IL-10-competent B cell differentiation.

48 rcised through the effectiveness of terminal B cell differentiation.

49 ate the role of PDK1 in early and peripheral B cell differentiation.

50 there was a disruption in erythropoiesis and B-cell differentiation.

51 II cells constitutes a crucial checkpoint in B-cell differentiation.

52 that impair the IL-21 signaling required for B-cell differentiation.

53 may play an adjunctive role in IL-21-induced B-cell differentiation.

54 The Sox4 transcription factor mediates early B-cell differentiation.

55 icular helper T (TFH) cells support terminal B-cell differentiation.

56 Chromatin remodeling is fundamental for B-cell differentiation.

57 IgH locus activity during the late stages of B-cell differentiation.

58 f wild-type PAX5, resulting in a blockade of B-cell differentiation.

59 oid priming, being selectively skewed toward B-cell differentiation.

60 ent in lyn(-/-) mice induces IL-10-producing B-cell differentiation.

61 ions as a key regulator of hematopoiesis and B-cell differentiation.

62 KDM6B may also have a role in antigen-driven B-cell differentiation.

63 m patients with CVID as a central pathway in B-cell differentiation.

64 10 genes is indeed stably established during B-cell differentiation.

65 c regulatory networks for erythropoiesis and B-cell differentiation.

66 factor regulating isotype-specific terminal B-cell differentiation.

67 withdrew from mitosis and underwent further B-cell differentiation.

68 valuate FcRH1 expression and function during B-cell differentiation.

69 e regulation, nervous system development and B-cell differentiation.

70 tes which are alternatively expressed during B-cell differentiation.

71 cells represents the critical final step in B-cell differentiation.

72 levels is an important step for myeloid and B-cell differentiation.

73 t occur only during the centroblast stage of B-cell differentiation.

74 tion and define a manipulable model of human B-cell differentiation.

75 d general processes throughout all stages of B-cell differentiation.

76 3 after undergoing isotype switch and memory B-cell differentiation.

77 to lymphomagenesis by blocking this terminal B-cell differentiation.

78 UBE2L3 genotype on NF-kappaB activation and B-cell differentiation.

79 receptor clustering, the first checkpoint of B-cell differentiation.

80 as well as in genes involved in myeloid and B-cell differentiation.

81 own about T-cell dysregulations that support B-cell differentiation.

82 ranscriptional program reminiscent of normal B-cell differentiation.

83 a transcription factor important for T- and B-cell differentiation.

84 artly compensate for loss of Btk activity in B cell differentiation, although the underlying mechanis

85 and natural killer cell compartment, whereas B-cell differentiation, although normal in number, was d

86 lts identify Itfg2 as a novel contributor to B cell differentiation and a negative regulator of the a

87 ell-mediated immune response as it regulates B cell differentiation and Ab production.

88 cells are specialized in providing help for B cell differentiation and Ab secretion.

89 The mechanisms that drive normal B cell differentiation and activation are frequently sub

90 terial colonization of the intestine induces B cell differentiation and activation.

91 te that FAIM is a new player on the field of B cell differentiation and acts as a force multiplier fo

92 the importance of this pathway in effecting B cell differentiation and associated molecular events s

93 elays germinal center involution and impedes B cell differentiation and class switch recombination.

94 ete DJ rearrangements can still revert their B cell differentiation and develop along myeloid lineage

95 ular protein and it plays a critical role in B cell differentiation and development of autoimmunity.

96 and the development of GCs, interfered with B cell differentiation and disrupted the development of

97 talk with B cells and affect IL-10-competent B cell differentiation and expansion.

98 l autophagy that is important in controlling B cell differentiation and fate.

99 It regulates B cell differentiation and function, promotes T follicul

100 ne protein 2A (LMP2A) interferes with normal B cell differentiation and function, we sought to determ

101 ic cytokine IL-21 has been shown to regulate B cell differentiation and function.

102 mplex, is one of multiple regulators driving B cell differentiation and germinal center (GC) formatio

103 tudies demonstrate that FCMR is required for B cell differentiation and homeostasis, the prevention o

104 The bone marrow provides niches for early B cell differentiation and long-lived plasma cells.

105 the factors that regulate antigen-activated B cell differentiation and memory cell formation has imp

106 Successful B cell differentiation and prevention of cell transforma

107 PPARgamma ligands can stimulate human B cell differentiation and promote Ab production.

108 (GCTfh) in lymphatic tissue are critical for B cell differentiation and protective antibody induction

109 entify Zbtb20 as an important player in late B cell differentiation and provide new insights into thi

110 ither BCR or TLR signaling, thereby allowing B cell differentiation and that the maintenance of Ets1

111 e Janus kinase/STAT5 pathway (ii) progenitor B-cell differentiation and (iii) the CDKN2A tumor-suppre

112 cko mice allowed the complete restoration of B-cell differentiation and a normal usage of the IgVkapp

113 Deletions of key B-cell differentiation and cell cycle control genes are

114 s and their signature cytokines in mediating B-cell differentiation and class switch recombination.

115 B-cell samples that comprise the spectrum of B-cell differentiation and common malignant phenotypes.

116 The ability of TEL-AML1 to block B-cell differentiation and downregulate the IRF3-IFNalph

117 tion factors IRF4 and IRF8, each critical to B-cell differentiation and fate.

118 f the predicted genes, 63.4% have defects in B-cell differentiation and function and 22% have a role

119 ability of ERT and HSC-GT to restore normal B-cell differentiation and function.

120 g enhancer activity, thus causing defects in B-cell differentiation and function.

121 A in hematopoietic progenitor cells promoted B-cell differentiation and induced the expression of B-c

122 ory program in the bone marrow that promotes B-cell differentiation and inhibits the development of B

123 est that the mutant protein has an effect on B-cell differentiation and is likely a monogenic cause o

124 epigenetic regulators such as miRNAs during B-cell differentiation and lymphomagenesis, and recent a

125 fied opposing roles for mTORC1 and mTORC2 in B-cell differentiation and showed that TOR-KIs enhance c

126 r CXCR4 mutations corresponded to diminished B-cell differentiation and suppression of tumor suppress

127 tween epigenetic alterations associated with B-cell differentiation and the acquisition of somatic mu

128 a role with important implications for both B-cell differentiation and the pathogenesis of B-cell ma

129 tion in murine B cells leads to an arrest in B-cell differentiation and the subsequent development of

130 h Rbm15 has been reported to be required for B-cell differentiation and to inhibit myeloid and megaka

131 to ensure the survival of host cells during B cell differentiation, and contribute to the developmen

132 and escape of infectious pathogens, in T and B cell differentiation, and in tumor defense.

133 of a B-cell-specific genetic program and for B-cell differentiation, and also to suppress genes of al

134 T T(FH) cells reconstituted GC formation, GC B-cell differentiation, and LN cell survival.

135 d in BHD syndrome is absolutely required for B-cell differentiation, and that it functions through bo

136 together with severely disturbed peripheral B-cell differentiation, apparently leads to a defective

137 er the physiologic signals that drive normal B-cell differentiation are absent in EBV-transformed cel

138 ivation of the secretory poly(A) site during B-cell differentiation are changes in the binding of cle

139 We demonstrate that TEL-AML1 induces a B cell differentiation arrest, and that leukemia develop

140 uggesting that CTCF levels may contribute to B-cell differentiation as well as EBV latency type deter

141 profiles in B-cell subsets during peripheral B-cell differentiation as well as in diffuse large B-cel

142 Positive selection is required for B cell differentiation, as indicated by the requirement

143 Defects in these genes result in a block in B cell differentiation at the pro-B to pre-B cell transi

144 , it appears that Notch regulates peripheral B cell differentiation, at least in part, through opposi

145 of RA susceptibility with genes involved in B cell differentiation (BACH2) and DNA repair (RAD51B).

146 on sufficient levels of IL-7 than precursor B cell differentiation because the number of B cells and

147 emonstrate distinct regulatory mechanisms in B cell differentiation between adults and children with

148 from these receptors is sufficient to drive B cell differentiation beyond the pre-B and immature B c

149 Hence, aside from its role in B-cell differentiation, Blimp-1 directs restraint among

150 fect the pre-B-cell receptor result in early B-cell differentiation blockades that lead to primary B-

151 not appear to be required for commitment to B cell differentiation but is crucial for B cell differe

152 utoimmunity because a possible modulation of B cell differentiation by basophils could point to new t

153 mice, suggesting that sIgM regulate splenic B cell differentiation by decreasing BCR signaling.

154 Rather, Ras promotes STAT5-dependent pro-B cell differentiation by enhancing IL-7Ralpha levels an

155 these studies suggest that Spi-C may promote B cell differentiation by modulating the activity of PU.

156 eased SP110 protein levels and impaired late B-cell differentiation cause VODI and that the condition

157 tand the function of GON4L, we characterized B cell differentiation, cell cycle control, and mitotic

158 ma and diffuse large B-cell lymphoma with GC B-cell differentiation, confirming previous microarray g

159 ting IgH function during the early phases of B cell differentiation, consistent with the view that co

160 ossibility that redundancies in pathways for B cell differentiation could be further revealed by elim

161 The terminal stage of B cell differentiation culminates in the formation of pl

162 at confer lupus susceptibility may influence B cell differentiation depending on their Ag specificity

163 y-state or regenerative hematopoiesis and in B-cell differentiation despite the fact that MLL1 is cri

164 y RNAs and upregulated genes associated with B-cell differentiation (e.g., C2TA, HLA-II, IL21R, MIC2,

165 in Xenopus but also suggests another role in B cell differentiation earlier in ontogeny.

166 Although Bach2 has a well-described role in B cell differentiation, emerging data show that Bach2 is

167 ator OCA-B is required for antigen-dependent B cell differentiation events, including germinal center

168 Although originally identified as a B cell differentiation factor, it is now known that mamm

169 Genomic alterations in B cell differentiation factors such as PAX5, IKZF1, and

170 sequential switching are linked to distinct B cell differentiation fates: direct switching generates

171 monstrates that Treg cells are important for B-cell differentiation from HSCs by maintaining immunolo

172 prevents the myeloid cell fate while driving B-cell differentiation from lymphoid-primed multipotent

173 ects showed increased expression of multiple B cell differentiation genes, and a set of just 3 of the

174 Upon IKAROS loss, expression of pre-B-cell differentiation genes is attenuated, while a grou

175 IKAROS defines superenhancers at pre-B-cell differentiation genes together with B-cell master

176 xo1 as a critical PI3K regulatory target for B cell differentiation has united membrane proximal regu

177 the BLNK protein's precise function in human B-cell differentiation has not been completely specified

178 Early B-cell differentiation has not been defined in patients

179 RDM1/Blimp-1, a master regulator in terminal B-cell differentiation, has been recently identified as

180 NF cytokine family, is a prominent factor in B cell differentiation, homeostasis, and selection.

181 H cell and B-cell cocultures, they inhibited B-cell differentiation, impeded immunoglobulin secretion

182 an important role of impairment of terminal B cell differentiation in DLBCL pathogenesis.

183 cells, and greatly increased germinal center B cell differentiation in dLNs compared with a combinati

184 In addition, STAT5 activation also restored B cell differentiation in IL7R(-/-) mice as determined b

185 Z microenvironment as a result of changes in B cell differentiation in mice lacking CD19.

186 d B cells cooperate for optimal T(FH) and GC B cell differentiation in response to both model Ags and

187 ogic DNA damage response signaling, promotes B cell differentiation in response to genotoxic stress.

188 During B cell differentiation in the bone marrow, the expressio

189 However, the intrinsic impact of RA on B cell differentiation in the regulation of gut humoral

190 Restoration of Ikaros function rescues pre-B cell differentiation in vitro and in vivo and depends

191 ally expressing vFLIP at different stages of B cell differentiation in vivo.

192 tes Id2 and Id3 mRNA expression and restores B cell differentiation in vivo.

193 n this study we evaluated the late stages of B-cell differentiation in a heterogeneous population of

194 is reduced Myc overexpression fails to block B-cell differentiation in resistant birds, while high My

195 However, the stages of B-cell differentiation in which disease can initiate and

196 romic enhancers become demethylated later in B-cell differentiation, in B and plasma cells.

197 xpression of known STAT3 targets involved in B-cell differentiation, including BLIMP-1, XBP-1, IL-6,

198 t become tumorigenic and fail to undergo pre-B cell differentiation induced by v-Abl inactivation.

199 BLIMP1, a key player in both epithelial and B-cell differentiation, induces reactivation of the onco

200 B cell differentiation into a plasma cell requires expre

201 Thus, human basophils modulate B cell differentiation into Ab-producing PC.

202 an drive B cell activation and contribute to B cell differentiation into Ab-secreting plasma cells.

203 B cell differentiation into antibody-secreting cells (AS

204 gnaling on DCs licensed the cells to promote B cell differentiation into class-switched plasmablasts

205 GLA-SE augments Ag-specific B cell differentiation into germinal center and memory p

206 lls with B cells, the former directly induce B cell differentiation into GraB cells.

207 n B cell maturation, yet its precise role in B cell differentiation into Ig-secreting cells (ISCs) re

208 rkers CD23 and CD40, which are important for B cell differentiation into IgG-producing PC.

209 Tight control of B cell differentiation into plasma cells (PCs) is critic

210 aintain them and to regulate germinal center B cell differentiation into plasma cells and memory B ce

211 tion factor, which is critical for promoting B cell differentiation into plasma cells, is repressed b

212 t the transcription factor Ets1 can restrain B cell differentiation into plasma cells.

213 /physiologic UPR components are required for B-cell differentiation into antibody-secreting cells, we

214 tor revision and class switching to IgE, and B-cell differentiation into IgE-secreting plasma cells i

215 ession levels of CD86, while only CT induced B-cell differentiation into plasma cells.

216 Mature B cell differentiation involves a well-established trans

217 When B cell differentiation is carried out ex vivo, CIITA sil

218 IgE(+) B cell differentiation is characterized by a transient G

219 Further B cell differentiation is dependent upon signals elicite

220 fferentiation of CD19(+) B-lineage cells and B cell differentiation is profoundly blocked beyond the

221 er, the role of A2aR in humoral immunity and B cell differentiation is unknown.

222 Although the importance of PI3K activity in B cell differentiation is well documented, the role of P

223 In addition, a role for osteopontin in B-cell differentiation is becoming clear.

224 We show that IRF4, an essential regulator of B cell differentiation, is critical for EBNA3C binding s

225 f these, CD40, provides critical signals for B cell differentiation, isotype switching, and B cell me

226 thin secondary lymphoid organs that promotes B-cell differentiation leading to antibody class-switch

227 re associated with dysregulation of terminal B-cell differentiation, leading to humoral immune defici

228 A regulation of key transcription factors in B-cell differentiation: LMO2 and PRDM1 (Blimp1).

229 lated by SOX11 including the block of mature B-cell differentiation, modulation of cell cycle, apopto

230 It is well accepted that Ag-induced B cell differentiation often results in the generation o

231 ing bystander T-B interactions can calibrate B cell differentiation outcomes.

232 demonstrate viral exploitation of the normal B cell differentiation pathway to maintain latency.

233 hin single cells at sequential stages in the B cell differentiation pathway.

234 dation of the complex mechanisms involved in B-cell differentiation pathways.

235 The B cell differentiation potential of HNF1A(-/-) common ly

236 utlined a novel role of iron in modulating a B cell differentiation process that is critical to the g

237 e for microRNAs at every stage of the mature B-cell differentiation process.

238 binding protein 1) that are critical to the B cell differentiation processes that underpin Ab and au

239 me of ten subpopulations spanning the entire B cell differentiation program by whole-genome bisulfite

240 nd that cognate iNKT cell help resulted in a B cell differentiation program characterized by extrafol

241 rhaps to prevent skewing of the conventional B cell differentiation program.

242 o tumor development by altering the terminal B-cell differentiation program of MCL and provide perspe

243 a role for these events in modifying normal B-cell differentiation programs and impeding germinal ce

244 In these mice, GC B cell differentiation, proliferation, and class switchi

245 d in vitro assays to routinely analyze human B cell differentiation, proliferation, and Ig production

246 Induction of these important regulators of B cell differentiation provides a possible mechanism for

247 Mature B-cell differentiation provides an important mechanism f

248 the likelihood of marginal zone (MZ) and B-1 B cell differentiation rather than just follicular (FO)

249 and downstream effectors of Ras that govern B cell differentiation remain undefined.

250 more specifically in shaping the outcome of B-cell differentiation, remains unclear.

251 d regulatory T cells, as well as intrathecal B-cell differentiation resulting in the generation of an

252 lls, which in turn leads to perturbations of B cell differentiation, resulting in dysregulated antibo

253 strated a block at exactly the same point in B cell differentiation (see the related article beginnin

254 neous B cell lymphoma specimens two specific B cell differentiation stage signatures of germinal cent

255 ociations with SPIB occupancy, signatures of B-cell differentiation stage and potential pathogenetic

256 The level of JAM-C expression defines B-cell differentiation stages and allows the classificat

257 matically modulated by pre-BCR signaling and B cell differentiation status.

258 gradually became demethylated during normal B-cell differentiation, suggesting that MM cells either

259 ed a number of the critical defects in early B cell differentiation that are seen in BLNK-deficient m

260 pression of an inherently mutagenic stage of B cell differentiation that gammaherpesviruses are thoug

261 r reaction, an inherently mutagenic stage of B cell differentiation that is thought to be the primary

262 the ability of CD4 memory T cells to support B-cell differentiation that was impaired in the elderly

263 on IL-7 of B cell precursor survival versus B cell differentiation, the combined effects of lack of

264 Despite enhanced germinal center (GC) B cell differentiation, the formation of GC structures w

265 p100 production emerged during transitional B cell differentiation, the stage at which BCR signals b

266 sion in primary B cells facilitates terminal B cell differentiation to ASCs.

267 ting small molecule can target two stages of B cell differentiation to dampen the pathogenic autoanti

268 ex reduced by approximately 70% human memory B cell differentiation to HPV 16 VLP IgG-secreting cells

269 ant roles for normal Ig production, terminal B cell differentiation to plasma cells, and Th17 differe

270 M2 has been shown to drive B cell differentiation to plasma cells, as well as inter

271 re differentially used at distinct stages of B cell differentiation to selectively control the abilit

272 to B cell differentiation but is crucial for B cell differentiation to the CD19(+) pro-B cell stage a

273 il the kinetics of CD40 ligand/IL-21-induced B-cell differentiation to define new biomarker sets for

274 IL)-6 is an attractive target as it promotes B-cell differentiation to plasma cells, is important for

275 B-cell differentiation to plasmablasts in vitro in respo

276 Ab production by 17-HDHA is due to augmented B cell differentiation toward a CD27(+)CD38(+) Ab-secret

277 boring LMP1 enhanced proliferation and drove B cell differentiation toward a plasmablast-like phenoty

278 IL-2 drove activated B cell differentiation toward PC independently of its pr

279 ultimers to T cell/B cell cultures redirects B cell differentiation toward plasma cells, indicating t

280 target X-box-binding protein 1 (XBP1) drive B-cell differentiation toward plasma cells and have been

281 al Galpha protein levels and is required for B cell differentiation, trafficking, and Ab responses.

282 B cell differentiation transcription factors in memory,

283 investigated the effects of CpG DNA on human B cell differentiation using highly purified B cell subs

284 ion of T cell differentiation, and prevented B cell differentiation via a GATA3-dependent mechanism.

285 RNAs (ncRNAs) deregulates genes involved in B cell differentiation via direct repression and post-tr

286 to the well-documented effect of NK cells on B cell differentiation via their ability to secrete IFN-

287 L-7-rich environments cooperate to drive pre-B cell differentiation via transcriptional programs that

288 TI host defense by acting at a late stage in B cell differentiation, via its regulation of terminal p

289 p-regulation of genetic programs involved in B cell differentiation was only modestly affected.

290 hat NK cells can modulate various aspects of B cell differentiation, we entertained the possibility t

291 ar processes and extrinsic cues required for B cell differentiation, we set up a controlled primary c

292 in primary EBV infection, and their role in B-cell differentiation, we studied the involvement of CD

293 Pro-B cell proliferation and small pre-B cell differentiation were fully rescued by expression

294 ate in the thymus by day 4, but no sites for B cell differentiation were seen until 3 weeks.

295 sistent with TLS organization, all stages of B-cell differentiation were detectable in most tumors.

296 l follicles and undergo germinal center (GC) B-cell differentiation, whereas activated IgG(+) memory

297 poral changes in the miRNA expression during B-cell differentiation with a highly unique miRNA profil

298 ky) mice present with a complete blockade of B-cell differentiation, with a leaky block in T-cell dif

299 functional roles of Notch signaling in human B cell differentiation within the germinal center (GC).

300 lized CD4(+) T cell subset that orchestrates B cell differentiation within the germinal centers and h