ライフサイエンスコーパス: mature B cell

1 ant genes and are generated through CSR in a mature B cell.

2 ytic leukaemia (CLL) is a clonal disorder of mature B cells.

3 o oncogenic translocations/amplifications in mature B cells.

4 were largely demethylated in pro-, pre-, and mature B cells.

5 n later stage B cells, including circulating mature B cells.

6 their ability to differentiate in vitro into mature B cells.

7 quences constructed by NextGen sequencing of mature B cells.

8 ts, and in IgH class switch recombination in mature B cells.

9 ulosclerosis in Jh mice, a strain that lacks mature B cells.

10 y of Hdac3 is required for the generation of mature B cells.

11 ovel function for IRF4 in the homeostasis of mature B cells.

12 clonal deletion fails to rescue survival of mature B cells.

13 vel: HSPCs, common lymphoid progenitors, and mature B cells.

14 g role for CAML in the long-term survival of mature B cells.

15 a CD19-Cre driver strain, we deleted PTIP in mature B cells.

16 a resulted in increased amounts of Foxp1 and mature B cells.

17 B-cell transition, leading to a reduction in mature B cells.

18 differentiation and functional reactivity of mature B cells.

19 impaired the development of transitional and mature B cells.

20 AFF is an important prosurvival cytokine for mature B cells.

21 homa-associated chromosome translocations in mature B cells.

22 ctivated in the neoplastic transformation of mature B cells.

23 which mediates cleavage of CD23 on distinct, mature B cells.

24 ine bone marrow cells blocked development of mature B cells.

25 e responses, and slightly reduced numbers of mature B cells.

26 cell receptor (BCR)-induced proliferation of mature B cells.

27 critical for the survival and maturation of mature B cells.

28 on in B-cell development or specifically in mature B cells.

29 previously described, a 2-fold reduction in mature B cells.

30 characterized by an increased compartment of mature B cells.

31 is essential for the homeostatic survival of mature B cells.

32 tribution to the survival and maintenance of mature B cells.

33 jor antibody isotypes on the surface of most mature B cells.

34 hrough Nod1 promotes competitive survival of mature B cells.

35 is a transmembrane glycoprotein expressed by mature B cells.

36 pacity of EML-TA cells to differentiate into mature B-cells.

37 tic changes that are conserved from HSPCs to mature B-cells.

38 me positive acute lymphoblastic leukemia and mature B-cell acute lymphoblastic leukemia using biologi

39 e in which Irf4 was conditionally deleted in mature B cells, after immunization with protein Ags or i

40 yk-deficient mice, the DKO mice can generate mature B cells, albeit at >20-fold reduced B cell number

41 d the expression of 109 lncRNAs in pro-B and mature B cells and 184 lncRNAs in acute lymphoblastic le

42 an inverse correlation between normal human mature B cells and bone marrow plasma cells from patient

43 urvival and homeostasis of normal peripheral mature B cells and chronic lymphocytic leukemia cells, r

44 ted in a severe loss and reduced lifespan of mature B cells and completely abrogated development of B

45 uch tRNA-derived fragment, cloned from human mature B cells and designated CU1276, in fact possesses

46 rt of the B-cell coreceptor and expressed by mature B cells and follicular dendritic cells.

47 onal BCR is essential for the development of mature B cells and has been invoked in the control of th

48 D20 mAbs that efficiently deplete endogenous mature B cells and homologous CD20+ primary lymphoma cel

49 LC3 subsets with levels intermediate between mature B cells and ILC2.

50 XLA patients lack mature B cells and immunoglobulin and experience recurre

51 so induced IgG Abs in BAFF-R KO mice lacking mature B cells and in mice deficient in interferon signa

52 8 null allele extinguished IgD expression on mature B cells and increased IgM.

53 EBI2 is expressed in mature B cells and increases in expression early after a

54 cius is unaffected, whereas development into mature B cells and migration from the bursa are blocked

55 the TNF receptor family, is expressed on all mature B cells and on most B-cell lymphomas.

56 tablishes that receptor editing can occur in mature B cells and raises the possibility that this may

57 3 is sufficient to trigger transformation of mature B cells and support the notion that p53 deficienc

58 eath and proliferation in antigen-stimulated mature B cells and that mutations in this switch represe

59 tion and mutation process takes place in the maturing B cell and is responsible for the diversity of

60 -)Mb1-Cre(+/-) mice were virtually devoid of mature B cells, and B220(+)CD43(+) B-cell progenitors ac

61 itch recombination (CSR) occurs in activated mature B cells, and causes an exchange of the IgM isotyp

62 Both CD20 and CD19 mAbs effectively depleted mature B cells, and CD19 mAb treatment depleted plasmabl

63 eficient CD19(-/-) mice, in mice depleted of mature B cells, and in mice treated with CD22 mAb to pre

64 crucial survival factor for transitional and mature B cells, and is a promising therapeutic target fo

65 self renew, continuously differentiate into mature B cells, and thereby maintain peripheral B cell h

66 uitously expressed adaptor protein, promotes mature B cell apoptosis.

67 Cancers arising from mature B cells are characterized by clonal production of

68 In normal adult mice, most mature B cells are enriched for Nod1 up-regulated cells,

69 udy, we used conditional deletion of Irf4 in mature B cells as well as wild-type and Irf4-deficient m

70 B-cell receptor (BCR)-mediated activation of mature B cells, as well as higher concentrations of plas

71 How then do mature B cells avoid making a TI-2-like response to mult

72 CD19(+)CD5(+)CD23(+)sIgdim expressing clonal mature B cells but also its highly variable clinical cou

73 entiation and proliferation of Ag-challenged mature B cells, but also during final maturation of deve

74 feration of B cell progenitors and activated mature B cells, but is dispensable for B cell survival.

75 plays an essential role in the activation of mature B cells, but less is known about the role of IL-4

76 These cells comprise up to 30% of mature B cells by 22 months.

77 owed in wild-type mice that were depleted of mature B cells by anti-CD20 before or different times af

78 evidence that the survival of BCR deficient mature B cells can be rescued by a single signaling path

79 ssociated with endemic Burkitt's lymphoma, a mature B cell cancer characterized by chromosome translo

80 Thus, malaria infection favors mature B cell cancers by eliciting protracted AID expres

81 In mature B cells, class switch recombination (CSR) generat

82 Mature B cells coexpress both IgM and IgD B-cell antigen

83 ch gammaherpesviruses may gain access to the mature B cell compartment by recurrent seeding of develo

84 in the differentiation and selection of the mature B cell compartment.

85 aB signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence o

86 F3B1 mutation) involvement could be found in mature B cells, consistent involvement at the pro-B-cell

87 Malignancies derived from mature B cells constitute the majority of leukemias and

88 In mature B cells, CSR deletes Cmu and replaces it with a d

89 muMT (mature B-cell deficient) mice were prone to AAA formatio

90 Previous work has shown that mature B cells depend upon survival signals delivered to

91 y what we believe to be a new key factor for mature B cell development and provide a rationale for ta

92 consistent with the signal-strength model of mature B cell development being extended to include stim

93 s in regulating lymphoid lineage commitment, mature B-cell development, and the GC response via disti

94 Mature B cell differentiation involves a well-establishe

95 ory role for microRNAs at every stage of the mature B-cell differentiation process.

96 Mature B-cell differentiation provides an important mech

97 ms regulated by SOX11 including the block of mature B-cell differentiation, modulation of cell cycle,

98 Upon antigen exposure, miR-155(-/-) mature B cells displayed significantly higher double-str

99 show that mice lacking both PU.1 and SpiB in mature B cells do not generate germinal centers and high

100 ed cytidine deaminase (AID) by Ag-activated, mature B cells during T cell-dependent germinal center r

101 6 is a transcriptional repressor required in mature B cells during the germinal center (GC) reaction.

102 bination treatment, although this related to mature B-cell engraftment in NOD.Cg-Prkdc(scid) IL2rg(tm

103 ull activation and complete demethylation of mature B cell enhancers.

104 urface TACI expression is usually limited to mature B cells, excess BAFF promotes the expansion of TA

105 Mature B-cell exit from germinal centers is controlled b

106 (IgD) is an enigmatic antibody isotype that mature B cells express together with IgM through alterna

107 These results suggest that residual, mature B cells expressing autoreactive BnAbs, like 2F5 a

108 T1, in contrast to follicular mature B cells, failed to express key NF-kappaB target g

109 ts identify IL-2 as a crucial early input in mature B cell fate commitment.

110 EML1 cells differentiate to mature B-cells following treatment with IL7; whereas EML

111 ons, the loss of the BCR can be tolerated by mature B cells for some time, whereas HC-deficient B cel

112 n of Notch2 by Fringe enzymes is critical to maturing B cells for accessing DL1 on vascular endotheli

113 Mice with inducible deletion of Cdc42 in mature B cells formed smaller germinal centers and had a

114 Like T1 cells, mature B cells from Btk- and c-Rel-deficient mice also f

115 om pediatric thymus, and compared these with mature B cells from fetal and pediatric bone marrow.

116 The development of mature B cells from hematopoietic stem cells is a strict

117 Activated mature B cells from wild-type, Unc93b1(3d/3d)-mutant, or

118 te the biologic effects of Btk inhibition on mature B-cell function and the progression of B cell-ass

119 To evaluate its role in mature B cell functions, a conditional gene deficiency i

120 is a transcriptional repressor required for mature B-cell germinal center (GC) formation and implica

121 a similar characterization of primary human mature B cells has been lacking.

122 AID) produces widespread somatic mutation in mature B cells; however, the extent of "off-target" DSB

123 ic region that controls BAFF-R expression in mature B cells (i.e., the TNFRSF13C promoter).

124 dies in melanoma, support the involvement of mature B cells in cutaneous immunity.

125 ought to be restricted to antigen-activated, mature B cells in germinal centers.

126 BIK is implicated in the selection of mature B cells in humans.

127 older mice we observe a major population of mature B cells in LNs and in the spleens of mice with hi

128 se the Cre/Lox approach to inactivate p53 in mature B cells in mice (referred to as "CP" B cells) and

129 Our data therefore reveal that precursors of mature B cells in NOD mice exhibit an altered migration

130 pleen and preferentially differentiates into mature B cells in response to Plasmodium yoelii infectio

131 where we defined pro-B, pre-B, and immature/mature B cells in the adult kidney.

132 down-regulated proapoptotic Bmf, unlike most mature B cells in the adult.

133 Alcohol consumption also decreased mature B cells in the blood.

134 ed significant, albeit incomplete, rescue of mature B cells in the bone marrow, peripheral blood, spl

135 ns in myeloma are thought to occur solely in mature B cells in the germinal center through class swit

136 uggest that IRF4 controls the positioning of mature B cells in the lymphoid microenvironments by regu

137 Mature B cells in the mutant mice displayed nuclear accu

138 lusion, Notch2HCS mutant mice have increased mature B cells in the MZ of the spleen.

139 etion of Spi1 and Spib resulted in a lack of mature B cells in the spleen and a block in B cell devel

140 in the thymus, and a selective reduction in mature B cells in the spleen and bone marrow.

141 the role of intrinsic expression of Cdc42 by mature B cells in their activation and function.

142 canonical NF-kappaB activation potentials in mature B cells in vivo.

143 pecific, BCR dependent signaling cascades in mature B cells in vivo.

144 atalytic subunit of Pol zeta, selectively in mature B cells in vivo.

145 erarchy, from stem cells, B-cell precursors, maturing B cells in the germinal center, and circulating

146 ability to assure the survival of mature and maturing B cells in the periphery stands out.

147 MEDI551, an anti-CD19 Ab that depletes mature B cells including plasma cells may offer a compel

148 ndin E2 triggers antibody class switching in mature B cells, increasing the levels of anti-alpha-Gal

149 In response to antigenic stimulation, mature B cells interact with follicular helper T cells i

150 P1 expression, and promotes the shift from a mature B cell into the initial plasmacytic differentiati

151 e homolog Blimp-1 promote differentiation of mature B cells into Ab-secreting plasma cells.

152 sed recruitment of dendritic cells (DCs) and mature B cells into the draining lymph nodes and the per

153 When a BCR on a mature B cell is engaged by its ligand, the cell becomes

154 ment, its role in the persistence of resting mature B cells is controversial.

155 The role of microRNAs in mature B cells is largely unknown.

156 s known about how this reservoir of infected mature B cells is maintained for the life of the host.

157 Survival of mature B cells is regulated by B cell receptor and BAFFR

158 ent development of B lineage precursors into mature B cells is stringently controlled by stage-specif

159 development, but whether it plays a role in mature B cells is unknown.

160 not only for multiple myeloma, but also for mature B cell leukemia and lymphoma.

161 ells, implying a role in the pathogenesis of mature B-cell leukemia.

162 Finally, K13 protected the mature B-cell line Ramos against anti-IgM-induced apopto

163 s an obligate dimer in B cells and regulates mature B cell lineage fate and humoral immune responses

164 ic Kap1-KO mice displayed reduced numbers of mature B cells, lower steady-state levels of Abs, and ac

165 By screening 269 mature B cell lymphoma biopsies, we also identified a so

166 any genes found as translocation partners in mature B cell lymphoma.

167 ed into patient care for various subtypes of mature B-cell lymphoma (e.g., ibrutinib, idelalisib).

168 cents treated on the French-American-British Mature B-Cell Lymphoma 96 (FAB LMB 96) trial.

169 Mantle cell lymphoma (MCL) is a mature B-cell lymphoma characterized by poor clinical ou

170 Seven patients (0.48%) presented mature B-cell lymphoma consisting of 6 DLBCL and 1 FL.

171 tantly, miR-217 overexpression also promotes mature B-cell lymphomagenesis; this is physiologically r

172 Mature B cell lymphomas arising as a result of deregulat

173 l rate, it modifies lymphomagenesis to favor mature B cell lymphomas that are AID dependent and show

174 PURPOSE OF REVIEW: Mature B-cell lymphomas bearing concurrent chromosomal r

175 sed in most MCL but is not detected in other mature B-cell lymphomas or normal lymphoid cells.

176 d to few ALL subtypes (e.g. TCF3-PBX1), most mature B-cell lymphomas rely on BCR signaling provided b

177 within murine HSPCs, and find that it causes mature B-cell lymphomas that lack Bcl6 expression and ta

178 may be involved in the pathogenesis of human mature B-cell lymphomas.

179 surface BCR expression is conserved in most mature B-cell lymphomas.

180 ilarly contribute to c-myc amplification and mature B-cell lymphomas.

181 rolase UCH-L1 is frequently overexpressed in mature B-cell malignancies and is a potent oncogene in m

182 ieve promising clinical responses in various mature B-cell malignancies and might also be useful in d

183 Survival and progression of mature B-cell malignancies depend on signals from the B-

184 Despite major therapeutic advances, most mature B-cell malignancies remain incurable.

185 iagnosis and guides therapeutic decisions in mature B-cell malignancies while enhancing our understan

186 bserved across a broad range of immature and mature B-cell malignancies, thereby providing a rational

187 ling is a successful therapeutic strategy in mature B-cell malignancies.

188 ractive novel strategy for treating selected mature B-cell malignancies.

189 cally, biologically and genetically distinct mature B-cell malignancies.

190 Mantle cell lymphoma (MCL) is a mature B-cell malignancy that continues to have a high m

191 ll prolymphocytic leukemia (B-PLL) is a rare mature B-cell malignancy that may be hard to distinguish

192 We also subjected mice deficient in all mature B cells (muMT mice) to renal I/R and found that t

193 Splenic marginal zone lymphoma (SMZL) is a mature B-cell neoplasm characterized by rather indolent

194 Hairy cell leukemia (HCL) is a chronic mature B-cell neoplasm with unique clinicopathologic fea

195 SHIP(-/-)) results in spontaneous and lethal mature B cell neoplasms consistent with marginal zone ly

196 ive evaluation of large series of aggressive mature B-cell neoplasms reveals recurrent chromosomal ab

197 ne alterations have been identified in other mature B-cell neoplasms that are usually associated with

198 c miRNA whose expression is lost in numerous mature B-cell neoplasms.

199 of high-grade (52.9%) and low-grade (47.1%) mature B-cell NHL in CSA was also significantly differen

200 th these prognostic factors in children with mature B-cell NHL.

201 re independent risk factors in children with mature B-cell NHL.

202 arge B-cell lymphoma (MLBL) represents 2% of mature B-cell non-Hodgkin lymphoma in patients </= 18 ye

203 1 years) compared with younger children with mature B-cell non-Hodgkin's lymphoma (NHL) have been his

204 Although mature B cell numbers were only mildly reduced, bone mar

205 4 end-ligation activity and severely reduced mature B cell numbers, Lig4(R278H/R278H) (Lig4(R/R)) mic

206 f their efforts to express SV40 T antigen in mature B cells of mice.

207 ced deaminase initiates isotype switching in mature B cells of secondary lymphoid structures.

208 ents involving lymphoid-myeloid progenitors, mature B cells, or T cells.

209 GS: AID is expressed in many malignancies of mature B-cell origin and contributes to the development

210 immature B cells occurred with conversion to mature B cells over time.

211 t positive histone epigenetic marks, and the mature B cells partially dedifferentiated, induced RAG-1

212 icroRNAs may be important in maintaining the mature B-cell phenotype in normal and malignant B cells.

213 igh-grade disease with a shift toward a more mature B-cell phenotype, increased cycling and gene expr

214 n the context of a normal immune system, the mature B cell pool is naturally maintained by the renewa

215 B cells are selected to enter the peripheral mature B-cell pool only if they do not bind (or bind lim

216 Mature B cell pools retain a substantial proportion of p

217 king PTPRZ, the proportion and number of the mature B cell population are reduced.

218 The presence of the mature B cell population correlates with enhanced IgG an

219 Memory B cells are a dynamic subset of the mature B cell population that in some cases can reenter

220 pression of CD10, CD24, and CD38 relative to mature B cell populations and are expanded in the periph

221 at T1 and later stages, resulting in reduced mature B-cell populations and reduced antigen-specific i

222 mphoma (DLBCL) genetically resemble specific mature B-cell populations that are blocked at different

223 ath, and that a Bcl2 transgene reconstitutes mature B-cell populations, respectively.

224 Fetal mature B cells predominantly used proximal V, D, and J g

225 an B cell culture is the capacity to support mature B cell proliferation.

226 , most patients exhibited complete total and mature B cell recovery, whereas memory B cell subsets re

227 critical stage in their development when the mature B cell repertoire is shaped.

228 nal unresponsiveness or anergy exists in the mature B-cell repertoire along a continuum, a fact that

229 cells during B lymphopoiesis and peripheral mature B cells, respectively.

230 of newly generated B cells and about 30% of mature B cells show some degree of autoreactivity.

231 resent, but we also found that Tec-deficient mature B cells showed increased activation, proliferatio

232 In the absence of Lyn, mature B cell signaling was greatly enhanced, whereas im

233 We show that mature B cell-specific PTEN overexpression enhances CSR.

234 ls specifically at the transitional to naive mature B cell stage in WAS subjects.

235 autoreactivity are mostly deleted before the mature B cell stage, but are positively selected and exp

236 and partial deletion at the transitional to mature B cell stage, but become Env(-) upon receptor edi

237 lation of GL transcription is delayed to the mature B-cell stage is presently unknown.

238 We have discovered a distinct mature B-cell subset that accumulates with age, which we

239 onal 1 (T1) stage and leads to a decrease in mature B cell subsets and deficits in T cell-dependent a

240 ) mice develop normal B1 and B2 immature and mature B cell subsets and have normal levels of naive se

241 CD21 and CD24 distinguishes transitional and mature B cell subsets in mice.

242 mprised of two major, functionally distinct, mature B cell subsets, i.e., follicular mature (FM) and

243 t profound humoral immunodeficiency and lack mature B cell subsets, mirroring deficiency of the cytok

244 imuli confer regulatory functions to various mature B-cell subsets but immature B-cell progenitors en

245 combined heavy-chain genes from immature and mature B-cell subsets in mice, we demonstrate a striking

246 ne mice, whereas they clearly populate 1% of mature B-cell subsets in VH125Tg/NOD mice.

247 LEF-1 specifically in CLL but not in normal mature B-cell subsets or after B-cell activation.

248 ion severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers cou

249 Mature B-cell subsets, immune responses, and memory B-ce

250 Despite sharing some features with other mature B-cell subsets, they are refractory to BCR and CD

251 oject (IGP) to identify unique biomarkers of mature B cell subtypes.

252 ne marrow data, CCAST also reveals two major mature B-cell subtypes, namely CD123+ and CD123- cells,

253 MAP kinase signaling pathway in BAFF-induced mature B cell survival and homeostatic maintenance of B2

254 which are also important for BAFF to promote mature B cell survival.

255 aB family of proteins in B-cell development, mature B-cell survival and B-cell function.

256 e found that, although the Igalpha-deficient mature B cells survive for >20 d in vivo, the HC-deficie

257 tion factor that is expressed exclusively in mature B cells, T-cell progenitors, and plasmacytoid den

258 Taken together, these data indicate that in mature B cells, Tec and Btk may compete for activation o

259 lower median percentages of transitional and mature B cells than age-matched healthy controls (P<0.00

260 el negative selection mechanism for deleting mature B cells that acquire reactivity to self-Ag.

261 mia (CLL) is a disease of an accumulation of mature B cells that are highly dependent on the microenv

262 ignancy characterized by clonal expansion of mature B cells that are resistant to apoptosis.

263 ymphocytic leukemia (CLL) is a malignancy of mature B cells that depend on host factors in the tissue

264 BM, but instead appear to be generated from mature B cells that exhaustively expand during the indiv

265 al activity, we conditionally deleted E3' in mature B cells that possessed Ed(-/-) alleles.

266 kappaB signaling was ablated specifically in mature B cells, the differentiation and/or persistence o

267 a critical role for Cdc42 in the motility of mature B cells, their cognate interaction with T cells,

268 ng by acute deletion of Pten specifically in mature B cells, thereby excluding the developmental impa

269 Although HRS cells are derived from mature B cells, they have largely lost their B cell phen

270 microbial products in promoting survival of mature B cells through up-regulated Nod1, providing a po

271 remia had increased proportions of activated mature B cells, tissue-like memory B cells and plasmabla

272 cy substantially enhanced the sensitivity of mature B cells to activation via the BCR, but minimally

273 role in adaptive immune response by enabling mature B cells to switch from IgM expression to the expr

274 The propensity of mature B cells to transform has been linked to their lon

275 s as a novel marker for this lymphoma across mature B-cell tumors, and support the distinction of NMZ

276 ng cell growth, were enriched in NMZL across mature B-cell tumors, functionally caused the loss of th

277 ca1(+)kit(+)flt3(-) HSC compartment generate mature B cell types in different proportions: CLPs and k

278 or the generation and maintenance of several mature B cell types.

279 Upon cross-linking of BCR, mature B cells undergo proliferation with an increase in

280 Because developmentally matured B cells undergo biologically programmed strand-s

281 Furthermore, upon enhancer loss, the mature B cells unexpectedly underwent reversible retrogr

282 Therefore, the effects of depleting all mature B cells using a potent CD20 mAb, or of depleting

283 ed 33% and then shifted to the nearly final (mature) B cell value by the cycling pre-B cell stage.

284 rentiation of immature into transitional and mature B cells via activation of Erk, likely through a p

285 mediate the development of transitional and mature B cells, we examined B cell development using a m

286 nase (PI3K), a major survival determinant in mature B cells, we indeed found that combining constitut

287 Mature B cells were chronically activated, leading to hy

288 Late pre-B and immature and mature B cells were decreased in the bone marrow of Ebf1

289 T cell-mediated anti-tumor immune responses, mature B cells were depleted from wild-type adult mice u

290 wed us to produce chimeric mice in which all mature B cells were derived entirely from IgG1-expressin

291 ll function in promoting T cell homeostasis, mature B cells were either acutely or chronically deplet

292 -I and preB-II, and decreased frequencies of mature B cells were observed in bone marrow aspirates of

293 40 and CD86 expression by B cells, iNKT cell-matured B cells were unable to drive proliferation of au

294 trics can be propagated developmentally into mature B cells where they generate new DSBs downstream o

295 Similar to resting mature B cells, where the B-cell antigen receptor (BCR)

296 us human T cells expedites the appearance of mature B cells, whereas in vivo depletion of T cells ret

297 ch allowed us to generate all-iPSC mice from mature B cells, which have until now failed to support t

298 common leukemia in adults and arises from a mature B cell with either mutated or unmutated IGH@ tran

299 cell development but have reduced numbers of mature B cells with poor germinal centers, as well as in

300 D180 rapidly increased both transitional and mature B cells, with especially robust increases in tran