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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.
37 lular location for protein expression during B lymphocyte activation and the DNA damage response.
41 cells, to B cell lines or autologous primary B lymphocytes also promoted specific Ab-dependent NK cel
43 essential for class switch recombination in B lymphocytes and for sensitizing BRCA1-deficient tumour
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
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
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
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
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
68 with Artemis deficiencies do not have T- or B-lymphocytes and are diagnosed with severe combined imm
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
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
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
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
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
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
95 stone variant of human skeletal muscular and B-lymphocyte cells both derived from the ENCODE project.
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
101 stigated whether activated human circulating B-lymphocytes contributed to the secretion of MMPs.
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,
108 studies indicate transient BAFFR-Fc-mediated B lymphocyte depletion elicits long-term T1D protection
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
115 ng in patients with severe asthma, decreased B-lymphocyte development and hematopoietic progenitor ce
117 igate how transcription factor levels impact B-lymphocyte development, we generated mice carrying tra
124 d by arrested T-lymphocyte production and by B-lymphocyte dysfunction, which result in life-threateni
126 y maturation is a Darwinian process in which B lymphocytes evolve potent antibodies to encountered an
128 ve immune system due to the absence of T and B lymphocytes, experienced rates of stenosis comparable
132 BCR signaling were increased in precancerous B lymphocytes from Emu-myc mice compared with wild-type
136 mice lacking CLCa, the major CLC isoform in B lymphocytes, generating animals with CLC-deficient B c
139 e studies suggest that beta-glucan-activated B lymphocytes have an important and novel role in fungal
143 terized by the expansion of malignant CD5(+) B lymphocytes in blood, bone marrow, and lymphoid organs
145 ling is a hallmark feature of the neoplastic B lymphocytes in chronic lymphocytic leukaemia (CLL).
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
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
155 al role for WAS protein (WASP) expression in B lymphocytes in the maintenance of immune homeostasis.
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
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
164 ssociated herpesvirus (KSHV) has tropism for B lymphocytes, in which it establishes latency, and can
166 on induces the circulation of virus-specific B lymphocytes, including memory B cells that differentia
168 roles in the biology of normal and malignant B lymphocytes, including the modulation of the transform
170 rk centered on the transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp1).
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
177 nfection and disease; however, few models of B lymphocyte infection exist to study immune recognition
179 discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks a
181 e products cause human cancers and transform B lymphocytes into immortalized lymphoblastoid cell line
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
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
198 log) as primarily responsible for defects in B lymphocyte migration and antibody responses that accom
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
206 While EBV generally persists silently in B lymphocytes, periodic lytic (re)activation of latent v
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
215 rated by DC differed from those processed by B lymphocytes; PPI signal-sequence peptides were eluted
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
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
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
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,
235 EBVDeltaCTCF166 virus-immortalized primary B lymphocytes showed a decrease in LMP1 and LMP2A mRNA a
241 through production of growth factors such as B lymphocyte stimulator (BLyS; also known as "B-cell fac
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
247 ic monoclonal antibody specific for the CD20 B-lymphocyte surface antigen, has been increasingly adop
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
255 -term T1D protection by enriching regulatory B lymphocytes that are deleted by anti-CD20 cotherapy.
258 lecule-targeting approaches expanded CD73(+) B lymphocytes that exert regulatory activity suppressing
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
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
269 derived from Epstein-Barr virus-immortalized B-lymphocytes to verify that the hyperexcitability of DG
272 cule PRMT5 inhibitor that blocked EBV-driven B-lymphocyte transformation and survival while leaving n
276 e, we demonstrate that beta-glucan-activated B lymphocytes upregulate proinflammatory cytokines (TNF-
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
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
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
298 an peripheral blood (PB) IgM(+)IgD(+)CD27(+) B lymphocytes with somatically mutated IgV genes are con
300 on and reduced the frequency of anti-insulin B lymphocytes within the polyclonal repertoire of VH125T
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