ライフサイエンスコーパス: B-lymphocyte

1 ctors for thein vivocontrol of KSHV-infected B lymphocytes.

2 umerous cell types including endothelium and B lymphocytes.

3 c.a expression also confirmed in adult T and B lymphocytes.

4 quired for the generation and maintenance of B lymphocytes.

5 nly 10% of the exomic sequences expressed in B lymphocytes.

6 nt, but little is known about their roles in B lymphocytes.

7 discovered by elution from HLA-DR4 of pulsed B lymphocytes.

8 tional activation, and effector functions of B lymphocytes.

9 e of antigen receptor specificities in T and B lymphocytes.

10 enhanced BCR replacement in newly developed B lymphocytes.

11 transcriptomes of terminally differentiating B lymphocytes.

12 n, differentiation, and Ab secretion by IgM+ B lymphocytes.

13 p53 activity and the DNA damage response in B lymphocytes.

14 that promote growth and survival of infected B lymphocytes.

15 n in a proportion of developing anti-insulin B lymphocytes.

16 nform a tailored adaptive response via T and B lymphocytes.

17 SR in a cytokine-dependent fashion in mature B lymphocytes.

18 lobulin proteins, each specified by distinct B lymphocytes.

19 inducer of the costimulatory ligand CD86 on B lymphocytes.

20 promote the growth and survival of malignant B lymphocytes.

21 ed by the progressive accumulation of clonal B lymphocytes.

22 functions of various immune cells, including B lymphocytes.

23 whether Eos influence the biology of normal B lymphocytes.

24 cy (SCID) caused by a complete lack of T and B lymphocytes.

25 neri interacts with and occasionally invades B lymphocytes.

26 , in particular antibody-producing cells and B lymphocytes.

27 ually and combined in normal activated mouse B lymphocytes.

28 compartment, which is mainly formed by T and B lymphocytes.

29 ndent apoptosis in CLL cells, sparing normal B lymphocytes.

30 o stimulatory activity on BALB/c mice spleen B lymphocytes.

31 ting the developmental basis of diabetogenic B-lymphocytes.

32 in the generation and maintenance of mature B-lymphocytes.

33 nt to protect mice in the absence of CD4 and B-lymphocytes.

34 e shedding of Syndecan-4 from the surface of B-lymphocytes.

35 vels of circulating monocytes and T, but not B, lymphocytes.

36 We demonstrate that B-lymphocytes activated by un-methylated CpG motifs, fou

37 lular location for protein expression during B lymphocyte activation and the DNA damage response.

38 gestive protease, did not affect the induced B lymphocyte activation.

39 This was the only fraction to induce B-lymphocyte activation, since all the other fractions f

40 In activated B lymphocytes, AID initiates antibody variable (V) exon

41 cells, to B cell lines or autologous primary B lymphocytes also promoted specific Ab-dependent NK cel

42 B lymphocytes and CD4(+) and CD8(+) T lymphocytes were s

43 essential for class switch recombination in B lymphocytes and for sensitizing BRCA1-deficient tumour

44 cally expressed only in germinal center (GC) B lymphocytes and GC-derived lymphomas.

45 also associated with organized aggregates of B lymphocytes and gp38(+) fibroblasts, which resemble te

46 m-6 is CD45 negative, human peripheral blood B lymphocytes and human B cell line, Reh, with high CD45

47 -34-encoded IgMs from human peripheral blood B lymphocytes and human B cell lines, Reh, OCI-Ly8, and

48 bust engraftment with functional human T and B lymphocytes and human mast cells were found in signifi

49 ng effector cells, inducing regulatory T and B lymphocytes and immune deviation.

50 ulting in decreased production of peripheral B lymphocytes and impaired immune function.

51 enter and form viral replication centers in B lymphocytes and induce the proliferation of B cells.

52 a common gammaherpes virus with tropism for B lymphocytes and infection in immunocompetent individua

53 vivo mRNA delivery systems fail to transfect B lymphocytes and instead primarily target hepatocytes a

54 The TF BACH2 is essential for T and B lymphocytes and is associated with an archetypal super

55 th three distinct clusters of T lymphocytes, B lymphocytes and macrophages.

56 uned tropism of EBV for epithelial cells and B lymphocytes and may result in novel strategies for the

57 ct of SWCNTs on the number of T lymphocytes, B lymphocytes and monocytes within the PBMC subpopulatio

58 decrease of 23% in MHC class I expression on B lymphocytes and no change (+1.08%) in MHC class II exp

59 B-lineage cells (B lymphocytes and plasma cells) predominate in the infla

60 cupied BCR by mAb123 eliminates anti-insulin B lymphocytes and prevents type 1 diabetes.

61 ion involves antigen-presenting cells, T and B lymphocytes and results in the generation of allergen-

62 of flow cytometry sorting of antigen-binding B lymphocytes and single-cell reverse transcription poly

63 y and composition of monocytes, neutrophils, B lymphocytes and T cell subsets in lymphoid or mucosal

64 These data show that antigen-specific B lymphocytes and T lymphocytes are activated in piperac

65 PI3K activity is tightly regulated in T and B lymphocytes and that various defects in the PI3K-trigg

66 rated marked CD3-positive T-lymphocyte, mild B-lymphocyte and moderate macrophage infiltrates, with p

67 B-lymphocyte and myeloid chimerism were highly correlate

68 with Artemis deficiencies do not have T- or B-lymphocytes and are diagnosed with severe combined imm

69 ty through increased levels of soluble BAFF, B lymphocytes, and immunoglobulins.

70 late mRNA, navigate to the spleen, transfect B lymphocytes, and induce more than 60 pg of protein exp

71 ells, an increase in CD4(+) and CD8(+) T and B lymphocytes, and reduced B16 melanoma metastasis in th

72 ansplantation (HSCT) cures the T-lymphocyte, B-lymphocyte, and natural killer (NK)-cell differentiati

73 B lymphocytes are a key pathologic feature of multiple s

74 Autoreactive B lymphocytes are essential for the development of T cel

75 of immune tolerance, islet antigen-reactive B lymphocytes are known to play a crucial role in the de

76 letal system are tightly interconnected, and B lymphocytes are uniquely endowed with osteo-interactiv

77 Immunoglobulins (Ig) are produced by B lymphocytes as secreted antibodies or as part of the B

78 lacking both WASP and N-WASP selectively in B lymphocytes (B/DcKO).

79 Mice with conditional deficiency of Was in B lymphocytes (B/WcKO) have revealed a critical role for

80 h Epstein-Barr Virus (EBV) transformation of B-lymphocytes (B-cells), are a commonly used model syste

81 tissue macrophages) and CD8(+) T and CD21(+) B lymphocytes but not glandular epithelium.

82 KSHV establishes a latent reservoir within B lymphocytes, but few models exist to study KSHV-infect

83 5 is immunoprecipitated only from peripheral B lymphocytes, but not from Reh despite the high express

84 Latent infection of B lymphocytes by Epstein-Barr virus (EBV) in vitro resul

85 lstein immortalized antibody-producing mouse B-lymphocytes by fusion with myeloma cells.

86 capture ss-cell antigens allows autoreactive B-lymphocytes bypassing normal tolerance induction proce

87 ydrolase highly expressed in macrophages and B lymphocytes, catalyzes the degradation of palmitoyleth

88 bohydrates (I/i antigen) on erythrocytes and B lymphocytes, cause cold agglutinin disease, and are ca

89 did not exhibit the increase in bone marrow B lymphocytes caused by ovariectomy that occurred in con

90 s suggest an important role for transitional B lymphocytes (CD19 + CD24hiCD38hi) in promoting transpl

91 Cell-sorted CD45R(+) (predominantly B lymphocytes), CD4(+)/CD8(+) (T lymphocytes), and CD14(

92 and plasmacytoid dendritic cells, monocytes, B lymphocytes, CD4(+)CD25(high) regulatory T cells, and

93 r Brij 30, Span 20, and POESH using the DT40 B-lymphocyte cell line and two of its DNA-repair-deficie

94 of over 10 million 5-kb DNA segments in the B-lymphocyte cell line GB12878.

95 stone variant of human skeletal muscular and B-lymphocyte cells both derived from the ENCODE project.

96 C-X-C motif chemokine 13 (CXCL13) is a B lymphocyte chemoattractant that activates CXCR5.

97 During immune responses, B lymphocytes clonally expand and undergo secondary dive

98 nerated following beta-glucan stimulation of B lymphocytes, compared with the well-established TLR-9

99 tolerance and autoimmunity, primarily in the B lymphocyte context, are considered in some detail in t

100 In conclusion, circulating human B-lymphocytes contribute to the regulation of the innate

101 stigated whether activated human circulating B-lymphocytes contributed to the secretion of MMPs.

102 mediated homologous recombination, result in B lymphocyte death.

103 fined by decreased numbers of CD4 and memory B lymphocytes, decreased plasmacytoid dendritic cell num

104 ns, including those characteristic of T- and B-lymphocyte defects, are associated with CARD11, MALT1,

105 B lymphocytes; thus, CD20 depletion leads to B-lymphocyte deficiency.

106 Remarkably, chicken DT40 B lymphocytes deficient in POLD3 are viable and able to

107 Rituximab is a B lymphocyte-depleting agent used to treat lymphoma and

108 studies indicate transient BAFFR-Fc-mediated B lymphocyte depletion elicits long-term T1D protection

109 B lymphocyte depletion has little effect on bacterial nu

110 Despite eliciting broader B lymphocyte depletion, continuous combo therapy afforde

111 Unlike other B-lymphocyte-derived malignancies, which become dependen

112 f the Rag genes is tightly controlled during B lymphocyte development to prevent mistimed dsDNA break

113 bacterial polysaccharides during innate-like B lymphocyte development, through either natural exposur

114 the classical staining protocols to explore B lymphocyte development.

115 ng in patients with severe asthma, decreased B-lymphocyte development and hematopoietic progenitor ce

116 B-lymphocyte development in the bone marrow is controlle

117 igate how transcription factor levels impact B-lymphocyte development, we generated mice carrying tra

118 -dependent functions in normal and malignant B-lymphocyte development.

119 These preneoplastic B lymphocytes did not progress to detectable B lineage l

120 B-lymphocytes did not seem to have a major role in the s

121 verse environmental cues have been linked to B lymphocyte differentiation and activation.

122 from V, D, and J gene segments during early B-lymphocyte differentiation.

123 Unfortunately, the B lymphocyte-directed T1D interventions tested to date f

124 d by arrested T-lymphocyte production and by B-lymphocyte dysfunction, which result in life-threateni

125 onditioned media from beta-glucan-stimulated B lymphocytes elicited neutrophil chemotaxis.

126 y maturation is a Darwinian process in which B lymphocytes evolve potent antibodies to encountered an

127 TRPM7-deficient chicken DT40 B lymphocytes exhibit a strongly impaired SOCE compared

128 ve immune system due to the absence of T and B lymphocytes, experienced rates of stenosis comparable

129 B lymphocytes exploit macroautophagy to capture cytoplas

130 Proportions of B lymphocytes expressing CD73, an ecto-enzyme operating

131 The percentages of T and B lymphocytes expressing nuclear factor kappaB ligand (R

132 BCR signaling were increased in precancerous B lymphocytes from Emu-myc mice compared with wild-type

133 B lymphocytes from transient BAFFR-Fc-treated mice suppr

134 eplicates, covering more than 100,000 memory B lymphocytes from two healthy adults.

135 In latency reservoirs, such as B lymphocytes, gammaHVs exist as viral episomes and expr

136 mice lacking CLCa, the major CLC isoform in B lymphocytes, generating animals with CLC-deficient B c

137 The presence of tumor-infiltrating B lymphocytes has been linked to a favorable clinical ou

138 wever, their effect as direct stimulators of B lymphocytes has not been yet fully elucidated.

139 e studies suggest that beta-glucan-activated B lymphocytes have an important and novel role in fungal

140 veral novel targets for haptenation by AX in B lymphocytes have been identified.

141 B lymphocytes have critical roles as positive and negati

142 In B lymphocytes, Ig class switch recombination (CSR) is in

143 terized by the expansion of malignant CD5(+) B lymphocytes in blood, bone marrow, and lymphoid organs

144 re markedly expanded, whereas development of B lymphocytes in bone marrow is unaltered.

145 ling is a hallmark feature of the neoplastic B lymphocytes in chronic lymphocytic leukaemia (CLL).

146 Apoptotic B lymphocytes in contact with Shigella-IpaD are detected

147 Molecular analysis of B lymphocytes in LFs showed predominantly mono/oligoclon

148 ant signaling and for the proper position of B lymphocytes in lymphoid organs.

149 keys, SGN-CD19B effectively depleted CD20(+) B lymphocytes in peripheral blood and lymphoid tissues c

150 is characterized by the accumulation of CD5+ B lymphocytes in peripheral blood, lymphoid organs and b

151 Here we show the functional role of B lymphocytes in response to C. jejuni in the chicken th

152 n in the spleen with significantly decreased B lymphocytes in senile APPswe, PS1M146V and TauP301L tr

153 of GILZ in mice leads to an accumulation of B lymphocytes in the bone marrow, blood, and lymphoid ti

154 eages, but resulted in a progressive loss of B lymphocytes in the circulation.

155 al role for WAS protein (WASP) expression in B lymphocytes in the maintenance of immune homeostasis.

156 sease characterized by infiltration of T and B lymphocytes in the pituitary gland.

157 ibly including tissue macrophages) and T and B lymphocytes in the presence of detectable inflammatory

158 lymphoid progenitors that differentiate into B lymphocytes in the spleen and are capable of contribut

159 for the efficient transformation of primary B lymphocytes in vitro and possibly in vivo The tumor su

160 01 B cell line in vitro, as well as in mouse B lymphocytes in vivo.

161 on of naturally occurring islet-infiltrating B-lymphocytes in NOD mice recognizing the neuronal antig

162 here is little information about the role of B-lymphocytes in the regulation of MMPs; consequently, h

163 blood T lymphocytes, but not neutrophils or B lymphocytes, in an in vitro flow assay.

164 ssociated herpesvirus (KSHV) has tropism for B lymphocytes, in which it establishes latency, and can

165 B-lymphocytes, in addition to their well-known function

166 on induces the circulation of virus-specific B lymphocytes, including memory B cells that differentia

167 re able to correct aberrantly spliced BTK in B lymphocytes, including pro-B cells.

168 roles in the biology of normal and malignant B lymphocytes, including the modulation of the transform

169 The transcriptional repressor B lymphocyte-induced maturation protein 1 (BLIMP1) is a

170 rk centered on the transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp1).

171 other key transcriptional regulators such as B lymphocyte-induced maturation protein 1.

172 We report that B lymphocyte-induced maturation protein-1 (Blimp-1), a c

173 nscriptional regulator of PC differentiation B lymphocyte-induced maturation protein-1 (BLIMP-1), and

174 CD28 signaling in LLPC modulates the central B lymphocyte-induced maturation protein-1 transcriptiona

175 ly undescribed transcriptional regulation of B lymphocyte-induced maturation protein-1, a key mediato

176 B-lymphocyte-induced maturation protein 1 (Blimp1) is a

177 nfection and disease; however, few models of B lymphocyte infection exist to study immune recognition

178 Here, we developed a model of B lymphocyte infection with KSHV in which infected tonsi

179 discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks a

180 Transgenic peripherin autoreactive B-lymphocytes infiltrate NOD pancreatic islets, acquire

181 e products cause human cancers and transform B lymphocytes into immortalized lymphoblastoid cell line

182 e1 mice and inhibited the differentiation of B lymphocytes into plasma cells.

183 Infiltration of B lymphocytes into the subepithelial tissue of the lungs

184 The activation of naive B lymphocyte involves rapid and major changes in chromat

185 Senescence of T and B lymphocytes is a striking finding, which has recently

186 nfections therefore norovirus replication in B lymphocytes is not essential for infection.

187 The development and function of B lymphocytes is regulated by numerous signaling pathway

188 ological conditions, and RANKL production by B lymphocytes is required for the bone loss caused by es

189 esults demonstrate that N-WASP expression in B lymphocytes is required for the development of autoimm

190 A less known function of B lymphocytes is their ability to respond directly to in

191 RNA, present in stress granules in activated B lymphocytes, is released upon DNA damage and is transl

192 Cas9 gene editing revealed that both BTK and B lymphocyte kinase (BLK) are relevant targets of ibruti

193 ng of MRN in cancer, we engineered mice with B lymphocytes lacking MRN, or harboring MRN in which MRE

194 How B lymphocytes, lacking any known form of caveolin, repai

195 In B lymphocytes latently infected with KSHV, specific inhi

196 activation, with an emphasis on myeloid and B lymphocyte lineages.

197 equent membrane injury and repair can impair B lymphocyte-mediated immune responses.

198 log) as primarily responsible for defects in B lymphocyte migration and antibody responses that accom

199 t a functional role of the MIF-CXCR7 axis in B-lymphocyte migration.

200 ablative conditioning recipients have better B-lymphocyte/myeloid chimerism and are free from immunog

201 cells, including hepatic macrophages, T and B lymphocytes, natural killer cells and platelets, as we

202 xquisite controls over its host cells, human B lymphocytes, not only directing these cells during lat

203 ave identified 25,270 MAPs isolated from the B lymphocytes of 18 individuals who collectively express

204 irus (EBV) establishes lifelong infection in B lymphocytes of most human hosts and is associated with

205 renin throughout development and possesses a B-lymphocyte pedigree.

206 While EBV generally persists silently in B lymphocytes, periodic lytic (re)activation of latent v

207 B lymphocytes play a key role in type 1 diabetes (T1D) d

208 B lymphocytes play an essential regulatory role in the a

209 In NOD mice and also likely humans, B lymphocytes play an important role as APC-expanding au

210 T-cells in NOD mice and also likely humans, B-lymphocytes play an additional key pathogenic role.

211 ural immunoglobulin derived from innate-like B lymphocytes plays important roles in the suppression o

212 plicates in the throat, and then invades the B lymphocyte pool through a growth-transforming latent i

213 juni in the chicken through depletion of the B lymphocyte population (bursectomy) followed by challen

214 EILPs lacked efficient T and B lymphocyte potential but efficiently gave rise to NK c

215 rated by DC differed from those processed by B lymphocytes; PPI signal-sequence peptides were eluted

216 Moreover, IgM(+)IgD(+)CD27(+) B lymphocytes preferentially responded to neutrophil-der

217 We show in this study that stimulated, human B lymphocytes produce active TGF-beta1 from surface GARP

218 humans at future risk for T1D indicate that B lymphocytes producing them have undergone the affinity

219 s into neutrophils and monocytes but reduced B lymphocyte production in the bone marrow.

220 t, beta-glucan, unlike CpG, had no effect on B lymphocyte proliferation or IgM production.

221 th B/WcKO mice, B/DcKO mice showed defective B-lymphocyte proliferation and impaired antibody respons

222 factor 3 (TRAF3) regulates signaling through B-lymphocyte receptors, including CD40, BAFF receptor, a

223 B lymphocytes regulate several aspects of immunity inclu

224 Here we show that B lymphocytes repair PM wounds in a Ca(2+)-dependent man

225 Efficient ciliogenesis in chicken DT40 B lymphocytes required centrin2.

226 g of human postmortem tissue revealed that a B-lymphocyte response to stroke also occurs in the brain

227 Therefore, we tested the hypothesis that a B-lymphocyte response to stroke could contribute to the

228 e patients, suggesting that in some people a B-lymphocyte response to stroke may occur in the CNS.

229 gest that some stroke patients may develop a B-lymphocyte response to stroke that contributes to deme

230 However, the role of AngII in B lymphocyte responses is largely unexplored.

231 EBV infection of primary B lymphocytes resulted in global transcriptional repress

232 ease characterized by accumulation of clonal B lymphocytes, resulting from a complex balance between

233 PM7 with NS8593 or waixenicin A in wild-type B lymphocytes results in a significant decrease in SOCE,

234 In B lymphocytes, Ric-8A is essential for normal Galpha pro

235 EBVDeltaCTCF166 virus-immortalized primary B lymphocytes showed a decrease in LMP1 and LMP2A mRNA a

236 B lymphocyte-specific loss of Ric-8A did not compromise

237 To test its role in hematopoiesis and B lymphocytes specifically, we generated ric8 (fl/fl) va

238 Here, we explore how B lymphocytes stay in the race by expressing activation-

239 We have assessed the role of B lymphocyte stimulator (BLyS) and its receptors in the

240 B lymphocyte stimulator (BLyS) engenders survival and an

241 through production of growth factors such as B lymphocyte stimulator (BLyS; also known as "B-cell fac

242 Expression levels of B lymphocyte stimulator receptor 3 and programmed cell d

243 ctor of the TNF family (BAFF), also known as B lymphocyte stimulator, is a ligand required for the ge

244 a proliferation-inducing ligand (APRIL) and B-lymphocyte stimulator (BLyS), are important for the su

245 Tabulated data from T- and B-lymphocyte subset analysis and antidrug antibody respo

246 Chemokines engage B lymphocyte surface receptors, triggering heterotrimeri

247 ic monoclonal antibody specific for the CD20 B-lymphocyte surface antigen, has been increasingly adop

248 factor 3 (TRAF3) is a critical regulator of B lymphocyte survival.

249 B lymphocytes synthesizing these antibodies require help

250 These receptors (immunoglobulins in B lymphocytes, T cell receptors in T lymphocytes) are in

251 oietic subpopulations; 12% to 83% of non-ALL B lymphocytes, T cells, and/or myeloid cells harbored th

252 a patient presenting with a complete lack of B lymphocytes, T-cell lymphopenia, defective hematopoies

253 As a result of their pathogenic importance, B lymphocyte-targeted therapies have received considerab

254 This study therefore adds direct B lymphocyte targeting to the diversity of mechanisms us

255 -term T1D protection by enriching regulatory B lymphocytes that are deleted by anti-CD20 cotherapy.

256 Autoreactive B lymphocytes that commonly arise in the developing repe

257 Autoreactive B lymphocytes that escape central tolerance and mature i

258 lecule-targeting approaches expanded CD73(+) B lymphocytes that exert regulatory activity suppressing

259 ast majority of NHLs deriving from malignant B lymphocytes that express cell surface CD20.

260 characterized by an enrichment of regulatory B lymphocytes that inhibit T1D development through IL-10

261 e developed a model of KSHV-infected primary B lymphocytes that recapitulates features seen in PEL an

262 Here we show that in developing B lymphocytes, the RNA-binding proteins (RBPs) ZFP36L1 a

263 CD154 and stimulate the production of IgE by B lymphocytes through IL-25/IL-33 stimulation or TLR tri

264 tors can direct T cells to kill autoreactive B lymphocytes through the specificity of the B cell rece

265 xpressed during most developmental stages of B lymphocytes; thus, CD20 depletion leads to B-lymphocyt

266 that can block T1D development by converting B lymphocytes to a disease-inhibitory CD73(+) regulatory

267 The importance of B lymphocytes to present antigens for antibody productio

268 Epstein-Barr Virus (EBV) conversion of B-lymphocytes to Lymphoblastoid Cell Lines (LCLs) requir

269 derived from Epstein-Barr virus-immortalized B-lymphocytes to verify that the hyperexcitability of DG

270 In B lymphocytes, TRAF3 contributes to regulation of signal

271 es; abnormal serum Ig profiles; and aberrant B lymphocyte trafficking.

272 cule PRMT5 inhibitor that blocked EBV-driven B-lymphocyte transformation and survival while leaving n

273 Developing B lymphocytes undergo clonal expansion following success

274 Developing B lymphocytes undergo V(D)J recombination to assemble ge

275 B-lymphocytes undergo isotype switching, and IgM, IgG, a

276 e, we demonstrate that beta-glucan-activated B lymphocytes upregulate proinflammatory cytokines (TNF-

277 B lymphocytes use two DNA alteration mechanisms, class s

278 d the interactions of insulin-specific T and B lymphocytes using T cell and B cell receptor transgeni

279 mab (OFA), a human CD20-targeting mAb, kills B lymphocytes using the innate immune system including c

280 eficiency, and the pharmacologic ablation of B-lymphocytes using an anti-CD20 antibody, prevents the

281 ecific role of the inhibiting FcgammaRIIb on B lymphocytes (using CD19Cre mice) and in the myeloid ce

282 In B lymphocytes, Usp9X is required for the induction of PK

283 -transformed cells, not resting or activated B lymphocytes, validating it as an ideal therapeutic tar

284 oglobulin heavy and light chains from single B lymphocytes vary in efficiency, error rate and practic

285 ident FRCs established a favorable niche for B lymphocytes via production of the cytokine BAFF.

286 CpG methylation in isolated B lymphocytes was assayed on the Illumina HumanMethylati

287 HRV accumulation and replication inside the B lymphocytes was detected by a combination of in situ h

288 a known attenuator of p18(INK4c) function in B lymphocytes, was also able to bypass the requirement f

289 ll death occurring in Shigella-invaded CL-01 B lymphocytes, we provide evidence that the T3SA needle

290 ng ChIA-PET and Hi-C data derived from human B-lymphocytes, we demonstrate the effectiveness of 3D-GN

291 ection with KSHV in which infected tonsillar B lymphocytes were expanded by providing mitogenic stimu

292 C deficient only in B cells, indicating that B lymphocytes were the key cells affected by the absence

293 tecture drive typical gene rearrangements in B lymphocytes, whereas translocation hot spots and recur

294 V predominantly infects epithelial cells and B lymphocytes, which are the cells of origin for the EBV

295 We investigated EBV infection of resting B lymphocytes, which leads to continuously proliferating

296 In this study, we show that B lymphocytes with E2A that cannot be inhibited by calmo

297 We have treated B lymphocytes with either AX or a biotinylated analog (A

298 an peripheral blood (PB) IgM(+)IgD(+)CD27(+) B lymphocytes with somatically mutated IgV genes are con

299 The analysis of translocations from B lymphocytes with the method described here reveals the

300 on and reduced the frequency of anti-insulin B lymphocytes within the polyclonal repertoire of VH125T