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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

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