ライフサイエンスコーパス: B-cell differentiation

1 undergoing dynamic methylation during normal B cell differentiation.

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

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

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

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

6 rcised through the effectiveness of terminal B cell differentiation.

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

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

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

10 5; ERK; PI3K/Akt, and potently promote human B cell differentiation.

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

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

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

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

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

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

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

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

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

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

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

22 mperative to identify mediators that control B cell differentiation.

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

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

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

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

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

28 n essential component for understanding late B cell differentiation.

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

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

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

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

33 h locus are developmentally regulated during B cell differentiation.

34 phoid tissue displaying germinal centre (GC) B cell differentiation.

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

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

37 developmental defects at multiple stages of B cell differentiation.

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

39 transcription factors that are critical for B cell differentiation.

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

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

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

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

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

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

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

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

48 ranscriptional program reminiscent of normal B-cell differentiation.

49 a transcription factor important for T- and 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 Chromatin remodeling is fundamental for B-cell differentiation.

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

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

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

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

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

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

62 10 genes is indeed stably established during B-cell differentiation.

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

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

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

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

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

68 3 after undergoing isotype switch and memory B-cell differentiation.

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

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

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

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

73 cells, has been intensively investigated in B cell differentiation and Ab class switch.

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

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

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

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

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

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

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

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

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

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

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

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

86 tases downstream of the BCR is essential for B cell differentiation and function and is disturbed in

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

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

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

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

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

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

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

94 Successful B cell differentiation and prevention of cell transforma

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

96 dium infection and provide signals to direct B cell differentiation and protective antibody expressio

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

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

99 With HIV infection, B cell differentiation and regulatory markers are discre

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

101 receptor attenuates gammaherpesvirus-driven B cell differentiation and viral reactivation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 that are involved in driving such irrelevant B cell differentiation are not known.

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

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

131 enic progenitor proliferation, survival, and B-cell differentiation arrest, but not for normal B-cell

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

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

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

135 lular processes, including those involved in B cell differentiation, B cell receptor signalling, acti

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

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

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

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

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

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

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

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

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

145 e nucleosome remodeler Mi-2beta promotes pre-B-cell differentiation by providing repression capabilit

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

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

148 e evolutionary ages across the trajectory of B cell differentiation, consistent with epimutations ser

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

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

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

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

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

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

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

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

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

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

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

160 ase will help facilitate the manipulation of B cell differentiation for vaccine development or to tre

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

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

163 Epigenetic changes during B-cell differentiation generate distinct DNA methylation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 nal expansion, isotype switching, and memory B cell differentiation in response to T cell-independent

179 s of A20 in HSCs causes a severe blockade of B cell differentiation in the BM and absence of peripher

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

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

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

183 ta thus define the cell division kinetics of B cell differentiation in vivo, and identify the molecul

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

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

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

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

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

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

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

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

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

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

194 B cell differentiation into antibody-secreting cells (AS

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

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

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

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

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

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

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

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

203 These results establish extrafollicular B cell differentiation into short-lived AFCs as a key me

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

205 inhibition can ameliorate SLE by inhibiting B-cell differentiation into GCs.

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

207 that function as B-cell helpers, as well as B-cell differentiation into plasma cells and autoantibod

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

209 Mature B cell differentiation involves a well-established trans

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

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

212 The germinal center stage of B cell differentiation is important as both an amplifier

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 ect naive B cells and subsequently usurp the B cell differentiation process through the germinal cent

229 s cancer-associated pathogens that usurp the B cell differentiation process to establish life-long la

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

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

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

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

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

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

236 uires the downregulation of key genes in the B-cell differentiation program through an aPKC lambda/io

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

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

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

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

241 Mature B-cell differentiation provides an important mechanism f

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

243 ing of SLE: that it is a disease of aberrant B-cell differentiation rather than a defect in antigen-s

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

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

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

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

248 nique ability of gammaherpesviruses to usurp B cell differentiation, specifically, the germinal cente

249 sufficiency has broad deleterious effects on B-cell differentiation, specifically hampering gut lymph

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

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

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

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

254 ignaling for optimal affinity maturation and B-cell differentiation, supporting the need for immunogl

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

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

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

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

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

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

261 We applied SOMatic on a mouse pre-B cell differentiation time-course using controlled Ikar

262 viruses infect naive B cells and manipulate B cell differentiation to achieve a lifelong infection o

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

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

265 pulation of the germinal center response and B cell differentiation to establish lifelong infection i

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

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

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

269 tion-coupled APA (SCAP), is also executed in B cell differentiation to plasma cells.

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

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

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

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

274 B-cell differentiation to plasmablasts in vitro in respo

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

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

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

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

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

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

281 B cell differentiation transcription factors in memory,

282 c-Rel-deficient mice fully rescued terminal B cell differentiation, underscoring its critical B cell

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

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

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

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

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

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

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

290 To assess T-bet(CXCR3)(+) B-cell differentiation, we cultured B cells from MS pati

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

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

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

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

295 ranscriptional and epigenetic changes during B cell differentiation with cell division in vivo.

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

297 cessfully recapitulated the full spectrum of B-cell differentiation, with 4 discrete COO phases: earl

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