ライフサイエンスコーパス: B-lymphocyte

1 nal profiles of newly infected naive primary B lymphocytes.

2 rinsic defect in survival vs. wild-type (WT) B lymphocytes.

3 rived suppressor cells, and regulatory T and B lymphocytes.

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

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

6 ually and combined in normal activated mouse B lymphocytes.

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

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

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

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

11 umerous cell types including endothelium and B lymphocytes.

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

13 quired for the generation and maintenance of B lymphocytes.

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

15 numbers of CD4(+) T lymphocytes and CD20(+) B lymphocytes.

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

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

18 tional activation, and effector functions of B lymphocytes.

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

20 enhanced BCR replacement in newly developed B lymphocytes.

21 hways in nonmalignant versus malignant T and B lymphocytes.

22 as well as increased populations of CD73(+) B lymphocytes.

23 pports the prolonged survival of Traf3 (-/-) B lymphocytes.

24 ing a constitutively active CD30 receptor in B lymphocytes.

25 number of immune cells, including subsets of B lymphocytes.

26 ght chain amplicons and the transcriptome of B lymphocytes.

27 ferential requirement in immature and mature B lymphocytes.

28 pment, preimmune repertoire, and function of B lymphocytes.

29 the costimulation and activation of cognate B lymphocytes.

30 a strategy to track V(H)-D(H)J(H) motion in B-lymphocytes.

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

32 ting the developmental basis of diabetogenic B-lymphocytes.

33 n (AMR) treatment by targeting CD20 found on B-lymphocytes.

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

35 Upon activation by CD40 or TLR signaling, B lymphocytes activate NF-kappaB to induce activation-in

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

37 Total B-lymphocyte, activated B-cell, and plasmablast counts w

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

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

40 have accelerated T1D development, and PerIg B lymphocytes actively proliferate within islets and exp

41 Here, using genetically-modified DT40 B lymphocytes, along with various biochemical assays, in

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

43 showed that Lkb1, an understudied kinase in B lymphocytes and a major upstream kinase for Ampk, had

44 D3(+) T lymphocytes predominate over CD20(+) B lymphocytes and CD8(+) over CD4(+) T lymphocytes in AS

45 of human transcription factor TFIIH, in both B lymphocytes and epithelial cells, we hypothesized that

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

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

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

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

50 teins (LMPs), is expressed in newly infected B lymphocytes and in post-transplant lymphomas.

51 entral role in the self/nonself selection of B lymphocytes and in their activation by cognate antigen

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

53 The virus efficiently infects resting human B lymphocytes and induces their continuous proliferation

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

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

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

57 ntly expressed on the cell surface of mature B lymphocytes and is currently being studied as novel th

58 eosinophil activation but did enhance local B lymphocytes and macrophages and reduce neutrophils and

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

60 the repression of multiple gene programs in B lymphocytes and maintains the adult B-2 cell fate.

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

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

63 estraining PI3K/AKT signaling, and confining B lymphocytes and myelocytes within their dedicated func

64 CD23, the low-affinity IgE receptor found on B lymphocytes and other cells, contains a C-terminal lec

65 ) mice altered the BCR repertoire on hepatic B lymphocytes and resulted in reduced ANA and immune com

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

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

68 preferentially infects epithelial cells and B lymphocytes and sometimes T and NK lymphocytes.

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

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

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

72 B-lymphocyte and myeloid chimerism were highly correlate

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

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

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

76 oliferative fractions (PFs) of the malignant B lymphocytes, and its anomalous expression has been ass

77 the phenotypes of dendritic cells and T and B lymphocytes, and lead to exacerbated atherosclerosis o

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

79 CAR T cells targeting the B lymphocyte antigen CD19 have led to remarkable clinica

80 B lymphocytes are a key pathologic feature of multiple s

81 ource of diverse immunoglobulin repertoires, B lymphocytes are an indispensable part of humoral immun

82 Mature B lymphocytes are crucial components of adaptive immunit

83 B lymphocytes are important players of the adaptive immu

84 B lymphocytes are the major cellular reservoir in indivi

85 l survival were instead unaffected in normal B lymphocytes at the same BRB concentrations.

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

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

88 requencies of CD19+CD24hiCD38hi transitional B lymphocytes (Bregs) increased from a median of 6% befo

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

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

91 5 is immunoprecipitated only from peripheral B lymphocytes, but not from Reh despite the high express

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

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

94 B lymphocytes capture antigens from the surface of prese

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

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

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

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

99 lly infected biopsies indicated that CD20(+) B lymphocytes, CD8(+) T lymphocytes, and CD11c(+) cells

100 his work, we expressed TbIP(3)R in a chicken B lymphocyte cell line in which the genes for all three

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

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

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

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

105 displayed a significant decrease in hepatic B lymphocytes compared to untreated mice as assessed by

106 In Mdr2(-/-) mice, hepatic B lymphocytes constitutively produced IgG during fibrosi

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

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

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

110 ls have been found in the membranes of T and B lymphocytes contributing to key cellular events.

111 B-lymphocyte recovery, 5 had persistent low B-lymphocyte count and remained on intravenous immunoglo

112 y to determine the absolute T-lymphocyte and B-lymphocyte counts and the phenotypes of both T and B c

113 mediated homologous recombination, result in B lymphocyte death.

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

115 These results suggest an intrinsic B-lymphocyte defect in antibody production as well as an

116 In vitro stimulation of splenic B lymphocytes demonstrated decreased IgA, IgG, and IgM p

117 Flagellin's impact on the microbiota is B-lymphocyte dependent and, in humans, obese subjects ex

118 presents a new model of peripherin-reactive B lymphocyte-dependent autoimmune neuritis.

119 Further studies found transitory early B lymphocyte depletion delayed T1D onset in a portion of

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

121 B lymphocyte depletion has little effect on bacterial nu

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

123 evious phase 2 trials indicated benefit from B-lymphocyte depletion in myalgic encephalomyelitis/chro

124 ectious mononucleosis and cancers, including B lymphocyte-derived Burkitt lymphoma and immunocompromi

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

126 We also discuss recent insights into B lymphocyte development and attempt to synthesize seemi

127 B lymphocyte development and selection are central to ad

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

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

130 the classical staining protocols to explore B lymphocyte development.

131 examined intrinsic and extrinsic aspects of B-lymphocyte development and function.

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

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

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

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

136 plays a role in various cell types including B lymphocytes, differentiating neurons, endothelial cell

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

138 Although chiefly a B-lymphocyte disorder, several research groups have iden

139 d collaboration between islet-reactive T and B lymphocytes drives type 1 diabetes (T1D).

140 al that is linked to its latent infection of B lymphocytes, during which virus replication is not sup

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

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

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

144 At late stages, B lymphocytes exhibite an antigen-driven proliferation,

145 AMPKalpha1-deficient memory B lymphocytes exhibited aberrant mitochondrial activity,

146 y hematopoietic organs and that some splenic B lymphocytes express EdnrB.

147 BCR-transgenic model in which virtually all B lymphocytes express the H and L chain Ig molecules fro

148 However, adult Ezh2-deficient B lymphocytes expressed Lin28b, which encodes an RNA-bin

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

150 On the molecular level, T and B lymphocytes from both patients displayed low RhoA acti

151 Splenic B lymphocytes from EdnrB(NCC-/-) mice showed no intrinsi

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

153 on of a tumor virus, and 4) demonstrate that B lymphocytes from NOMID (neonatal onset multisystem inf

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

155 sk factors, and outcomes of post-HCT AIC and B-lymphocyte function following rituximab.

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

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

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

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

160 B lymphocytes have immunological functions beyond Ab pro

161 B lymphocytes have the ability to sense thousands of str

162 B lymphocytes have well-established effector roles durin

163 mediated inhibition of RXR Function, PI3K in B lymphocytes, iCOS-iCOSL in T helper cells, and the rol

164 rogenitors, but these cells maintained their B lymphocyte identity.

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

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

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

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

169 cullin 3 was identified to be important for B lymphocytes in general.

170 Yet, most B lymphocytes in humans and probably in other vertebrate

171 deletion of the tumor suppressor TRAF3 from B lymphocytes in mice leads to the prolonged survival of

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

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

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

175 ct, a large proportion of islet-infiltrating B lymphocytes in the NOD mouse model of T1D produce Abs

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

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

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

179 , essential for antigen recognition by T and B lymphocytes in viral-host interaction.

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

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

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

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

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

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

186 The transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp-1) has

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

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

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

190 d cells requires a transcriptional regulator B-Lymphocyte-Induced Maturation Protein 1 (BLMP-1/BLIMP1

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

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

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

194 ating the potential for productive cognate T-B lymphocyte interactions in T1D-prone mice.

195 tical intracellular signaling molecule for T-B lymphocyte interactions, drives T follicular helper (T

196 In vitro, EBV can transform primary human B lymphocytes into immortalized cell lines.

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

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

199 B-lymphocyte-intrinsic and -extrinsic defects in secreto

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

201 he maintenance of immunological tolerance of B lymphocytes is a complex and critical process that mus

202 e molecular mechanisms by which KSHV infects B lymphocytes is critical for understanding how the viru

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

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

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

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

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

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

209 In B lymphocytes latently infected with KSHV, specific inhi

210 ing and antibody synthesis, rare circulating B lymphocytes making pathogenic autoantibodies were foun

211 wild type or Rag knockout (lack mature T and B lymphocytes) male mice.

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

213 ies like healthy human cells (T-lymphocytes, B- lymphocytes, Monocytes, Leukocytes erythrocytes and h

214 B lymphocytes must respond to vast numbers of foreign an

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

216 ndings reveal novel functions of cullin 3 in B lymphocytes, namely regulating CD22 surface expression

217 ion and recruitment, together with a loss in B lymphocyte, natural killer and T cell effector respons

218 n a plasmacytoid dendritic cell-type I IFN-T/B lymphocyte network.

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

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

221 B lymphocytes play a central role in host immunity.

222 B lymphocytes play a critical role in adaptive immunity.

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

224 B lymphocytes play an essential regulatory role in the a

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

226 udies that highlight the important role that B lymphocytes play in cardiac and vascular disease.

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

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

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

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

231 Furthermore, because much of the B lymphocyte population is localized in organs or tissue

232 Mice developed expanded germinal center B lymphocyte populations as in other models of AID defic

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

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

235 l dysbiosis and a gut-specific deficiency of B-lymphocyte-produced secretory IgA (sIgA), the primary

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

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

238 ranscription factors, specifically in murine B lymphocyte progenitors, but these cells maintained the

239 Purified B lymphocytes proliferated normally but produced less im

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

241 -Barr virus (EBV) immortalization of resting B lymphocytes (RBLs) is a useful model system to study E

242 rus (EBV) infection of human primary resting B lymphocytes (RBLs) leads to the establishment of lymph

243 ng EBV transformation, primary human resting B lymphocytes (RBLs) were infected with B95.8 EBV for 0,

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

245 B lymphocyte reconstitution dominated by memory phenotyp

246 Of the 17 who received rituximab, 7 had B-lymphocyte recovery, 5 had persistent low B-lymphocyte

247 B lymphocytes regulate several aspects of immunity inclu

248 Antibody class switch recombination (CSR) in B lymphocytes replaces immunoglobulin heavy chain locus

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

250 riggers signaling pathways for commitment of B lymphocyte responses that can be regulated, in part, b

251 lls that are essential for most antibody and B lymphocyte responses.

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

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

254 DNAme in 22 primary CLL and 13 healthy donor B lymphocyte samples.

255 onses to kidney injury correlate with a late B lymphocyte signature relating to renal dysfunction and

256 s a pioneer transcription factor involved in B lymphocyte specification.

257 proval of belimumab, an mAb directed against B lymphocyte stimulation and the first targeted therapy

258 B lymphocyte stimulator (BLyS) engenders survival and an

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

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

261 However, function of STAT3 in the B lymphocyte subset is not well understood.

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

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

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

265 B-lymphocyte survival and Ig production were assayed in

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

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

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

269 Autoreactive B lymphocytes that escape central tolerance and mature i

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

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

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

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

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

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

276 explore alternative targets of autoreactive B lymphocytes through manipulation of affinity maturatio

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

278 ability to promote the continuous growth of B lymphocytes, thus providing significant new insight in

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

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

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

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

283 (i)-linked signaling pathways in controlling B lymphocyte trafficking.

284 Perturb-ATAC in human B lymphocytes uncovered regulators of chromatin accessib

285 Developing B lymphocytes undergo clonal expansion following success

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

287 B lymphocytes use two DNA alteration mechanisms, class s

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

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

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

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

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

293 ASp-deficient cell-pair model of human T and B lymphocytes, we show that WASp deficiency differential

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

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

296 crophages, CD4(+) T lymphocytes, and CD20(+) B lymphocytes were increased in all subjects.

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

298 eficiency (LAD) patient-derived immortalized B lymphocytes, where nearly 70% of alleles were repaired

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

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