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1 ty in the activation of the lineage germline B cell.
2 are significantly lower than in SPPL2a(-/-) B cells.
3 immune murine B cell subsets and CD27- human B cells.
4 ukaemia (CLL) is a clonal disorder of mature B cells.
5 rd antigen in activated germinal center (GC) B cells.
6 Ab, yet harbor marginal zone and follicular B cells.
7 ge pre-B cells to small B cells and immature B cells.
8 irus that establishes a latency reservoir in B cells.
9 ery of innate signals to antigen-experienced B cells.
10 ypermutation, and differentiated into memory B cells.
11 elated to their intracellular trafficking in B cells.
12 as impaired in all mature naive CVID-derived B cells.
13 CD4(+) and CD8(+) T cells but no binding by B cells.
14 c leukemia tumor cells while sparing healthy B cells.
15 ctivated memory cells and tissue-like memory B cells.
16 .IMPORTANCE EBV establishes viral latency in B cells.
17 e response and contained hypermutated IgD(+) B cells.
18 at concentrations that did not affect normal B cells.
19 urvival, and tissue infiltration of leukemic B cells.
20 late times for maintenance of the Tfh and GC B cells.
21 quencing method can use as few as 1000 naive B cells.
22 biting proliferation of germinal center (GC) B cells.
23 with less contribution from neutrophils and B cells.
24 o showed superior activation of Env-specific B cells.
25 s to sense alum and, in turn, activate T and B cells.
26 h cells than other lineages of more specific B cells.
27 (VL) sequences of individual and Ag-specific B cells.
28 ctor kappa-light-chain-enhancer of activated B cells.
29 c cells such as in mammalian hepatocytes and B-cells.
31 creased B regulatory cell [Breg] counts, and B cell activation and apoptosis) is specifically associa
32 s BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differentiation has implications f
34 into the RBC cell surface strongly inhibited B cell activation, cytokine secretion, and proliferation
35 d with an hCD22 ligand were shown to prevent B cell activation, increase cell death, and induce toler
39 phia chromosome (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to rec
40 d blood cancers and primary, patient-derived B-cell acute lymphoblastic leukemia blasts compared with
42 myeloid cells could contribute to the strong B-cell ALL association of MLL-AF4 leukemia observed in t
43 n, phosphoinositide-interacting protein 2 in B cells alone enhanced this noncanonical autophagy, resu
44 mmune responses by differentially regulating B cell and CD4 T cell responses during acute viral infec
45 fferences in function between MBCs and naive B cells and among MBC subsets and how this leads to memo
46 reported that NP contain elevated levels of B cells and antibodies, making NP an ideal system for st
47 that the IL-12p35 subunit induces regulatory B cells and can be used therapeutically to limit autoimm
48 ution to the gut, increases of the activated B cells and circulating tissue-like memory B cells, and
49 chromosomal rearrangements in primary murine B cells and discovered that RAG1/2 causes aberrant inser
50 eterogeneous expression of Ifnb in wild-type B cells and distinct gene expression patterns associated
53 on, we compared the fate of IgE-ICs in human B cells and in CD23-expressing monocyte-derived dendriti
54 ctor kappa-light-chain-enhancer of activated B cells and negative regulators tumor necrosis factor-al
55 e generated normal levels of germinal center B cells and plasmablasts in periphery, they produced sig
56 Pirfenidone dampened splenic germinal center B-cell and T-follicular helper cell frequencies that col
57 used a significant increase in percentage of B-cells and significantly decreased percentage of myeloi
58 d B cells and circulating tissue-like memory B cells, and expansion of the B regulatory cells (Bregs)
59 is comparable to expression on human primary B cells, and it colocalizes with mCD22 on the cell surfa
60 pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombinant chemokines us
61 ly composed of CD3+ T cells, scattered CD20+ B cells, and relatively few PD-1+ (programmed cell death
64 affinity-matured human NANP-reactive memory B cell antibodies elicited by natural Pf exposure that p
65 tion compromises the activity of the pivotal B-cell antigen receptor (BCR)-proximal effector spleen t
69 tter long-term outcome had higher numbers of B cells at birth than those who developed LTI; no differ
71 complex 1-dependent canonical autophagy, GC B cell autophagy occurred predominantly through a noncan
75 c antigen receptor (CAR) that target CD19 in B-cell cancers, although data regarding B-cell lymphomas
76 responses depend on competitive selection of B cells carrying somatically mutated B-cell receptors by
77 proportional decrease in splenic follicular B cells (CD21/35(int)CD23(+)) at 1, 2, and 12 months of
78 ed post-ART, with the frequency of activated B cells (CD86(+)CD40(+)) reduced compared with pre-ART l
80 nmutated common ancestor knock-in mice Env(+)B cell clones develop anergy and partial deletion at the
81 ne of the main factors limiting entry of new B cell clones into ongoing immunization-triggered GC res
91 ed to lethality in infected animals, whereas B cell-deficient mice showed CD4(+) T cell loss but reco
92 old reduced I-A expression on the surface of B cells, dendritic cells, cortical thymic epithelial cel
95 lly removed the pericardial AT and performed B-cell depletion and granulocyte-macrophage colony-stimu
96 circulating Ab in mediating CTL responses to B cell-derived exosomes was ruled out using DHLMP2A mice
97 data indicate that the environment in which B cells develop can affect the expressed Ig repertoire b
99 sitional B cell subsets demonstrated that MZ B cell development was blocked at the transitional-1 to
100 s the BCR and coreceptor programs throughout B cell development, promoting enrichment of self-reactiv
102 artly compensate for loss of Btk activity in B cell differentiation, although the underlying mechanis
103 ntial signaling and provide insight into how B cells discriminate between antigens of different quant
104 n both disease models, IL-4Ralpha-responsive B cells displayed increased IL-4 production as early as
105 oss of naive B cells, loss of resting memory B cells due to their redistribution to the gut, increase
106 E We report here that the HIV/SIV-associated B cell dysfunction (defined by loss of total and memory
108 onstitute a rate-limiting checkpoint against B cell dysregulation by MYD88(L265P) and provide an expl
111 p in this process is the activation of naive B cells expressing germline (gl) antibody precursors tha
115 decrease in the messenger RNA level of early B cell factor 1 (EBF1) and paired box 5, two critical tr
117 innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mecha
119 r helper (pTfh) cells, which provide help to B cells for developing into Ab-secreting cells, were sim
123 vate EBV lytic induction in freshly isolated B cells from peripheral blood mononuclear cells (PBMCs)
124 n that six codons in VH4-containing genes in B cells from the cerebrospinal fluid of patients with re
126 ranscriptomes and proteomes of primary mouse B cells from wild-type and STAT6-deficient mice cultured
127 ts on nonmotile E. coli exposed to polymyxin B, cell-generated frequency noise dropped close to zero
128 onal epitope(s), masked in refp17, to elicit B-cell growth-promoting signals after its interaction wi
131 PRIL system is best known for its control of B cell homeostasis, and it is a target of therapeutic in
132 expansion of the "exhausted," virus-specific B cells, i.e., activated memory cells and tissue-like me
135 estions about the establishment of effective B cell immunity elicited by vaccination, not just agains
138 omotes chronic gammaherpesvirus infection of B cells.IMPORTANCE Gammaherpesviruses infect a majority
143 later found to be present on some subsets of B cells in humans; however, whether CD6 plays any role i
145 een reported to respond against EBV-infected B cells in the lytic cycle and to control the viral infe
146 ur data suggest that the altered response of B cells in tolerant recipients may contribute to long-te
147 unction (defined by loss of total and memory B cells, increased B regulatory cell [Breg] counts, and
149 the clonal selection of high affinity memory B cells into the plasma cell fate, our findings provide
150 Expression of hCD22 on transgenic murine B cells is comparable to expression on human primary B c
151 t the block of CD74 degradation in CatS(-/-) B cells is incomplete, so that NTF levels are significan
153 transduced T cells efficiently lysed primary B-cell leukemia, mantle cell lymphoma, and multiple myel
154 300 are recurrently mutated in the activated B cell-like and germinal center (GC) B cell-like subtype
155 tivated B cell-like and germinal center (GC) B cell-like subtypes of diffuse large B cell lymphoma (D
156 e therefore expected to evolve only when the B cell lineage evolving breadth is consistently capturin
158 omic and epigenomic study in patient-derived B-cell lines to investigate the genome-scale effects of
159 infection is characterized by loss of naive B cells, loss of resting memory B cells due to their red
160 ignificantly higher prevalence of monoclonal B cell lymphocytosis, premalignant condition poorly desc
162 ly, BCL-W was overexpressed in diffuse large B cell lymphoma and correlated with decreased patient su
164 mphomas (DELs) are subtypes of diffuse large B-cell lymphoma (DLBCL) associated with poor outcomes af
166 licular lymphoma (FL; n = 29), diffuse large B-cell lymphoma (DLBCL; n = 34), DLBCL arising from chro
167 pression of downstream genes, such as Bcl-2 (B-cell lymphoma 2), c-Myc, MMP7 (matrix metalloproteinas
168 B-cell activation seemed to play a role in B-cell lymphoma development at early stages across diffe
169 CTL019) to treat patients with diffuse large B-cell lymphoma or follicular lymphoma that had relapsed
171 ous NHL histologies, including diffuse large B-cell lymphoma, Richter's transformation, mantle cell l
176 ed by mutations in JAK2, CALR, or MPL In the B-cell lymphomas, detection of characteristic rearrangem
177 lymphoma, Burkitt's lymphoma, diffuse large B-cell lymphomas, nasopharyngeal carcinoma (NPC), and ly
178 be a crucial part of the pathophysiology of B-cell lymphomas; however, several early attempts to tar
182 cal functions of BACH2 and its regulation of B-cell malignancies in chronic hypoxic microenvironment
183 these data and mutations identified in other B-cell malignancies, 1716 genes were sequenced in 113 FL
184 te (ADC) being investigated for treatment of B-cell malignancies, which has improved potency compared
186 fusion lymphoma (PEL) is a highly aggressive B-cell malignancy that is closely associated with one of
187 V/SIV infections and suggest that monitoring B cells may be a reliable approach for assessing disease
188 B-blasts can differentiate to become memory B cells (MBC), in which EBV persistence is established.
189 Myasthenia gravis (MG) is a prototypical B cell-mediated autoimmune disease affecting 20-50 peopl
192 not a consequence of diminished formation of B cell memory; instead, SpA reduced the proliferative ca
193 on that CD19-independent factors drive early B cell mobilization and recruitment to the infected CNS,
194 0-positive cells did not display the typical B cell morphology, having in general a more dendritic ce
195 hallmark anti-CD20 mAb for the treatment of B cell neoplasms, including B cell chronic lymphocytic l
196 nscriptional regulator Ikaros into mouse pre-B cell nuclei triggered immediate binding to target gene
198 Flow cytometric analysis of peripheral blood B cells of 30 MC-negative HCV-infected patients and 15 h
200 increase in CD21/35(high)CD23(-) splenic MZ B cells of approximately fivefold and a proportional dec
202 t higher proportions of IgM+CD21-/low memory B cells (P < .05), CD4+IFNgamma+ cells (P < .01), CD4+IL
203 on Network Analysis (WGCNA) was enriched for B cell pathways, and shared seventeen genes with a mouse
204 received renewed interest as an innate-like B cell population of fetal-derived hematopoiesis, respon
206 use in patients with relapsed or refractory B-cell precursor ALL on the basis of single-group trials
207 erimental stroke prevents loss of splenic MZ B cells, preserves IgM levels, and reduces bacterial bur
208 icial substrates or live cells, we show that B cells primarily use force-dependent extraction and res
209 s, mTORC1 activation is required for fueling B cells prior to DZ proliferation rather than for allowi
212 patient suffering from recurrent EBV-induced B cell proliferations including Hodgkin's lymphoma becau
213 ic cells are stiff cells that promote strong B cell pulling forces and stringent affinity discriminat
214 ted with 2 or more mutations, and linked the B cell receptor (BCR) pathway to trisomy 12, an importan
217 of infiltrating immune cell types, the T or B cell receptor repertoire, and direct the design of a p
219 ese B-ALLs encode proteins implicated in pre-B-cell receptor (BCR) signaling and migration/adhesion,
220 ated to regulate signaling downstream of the B-cell receptor (BCR), Fc receptors (FcRs), and toll-lik
221 ltage-gated proton channel-encoding gene and B-cell receptor signaling modulator, were associated wit
223 tion of B cells carrying somatically mutated B-cell receptors by follicular helper T (TFH) cells in g
224 ever, intravital imaging suggests that early B-cell recognition of large foreign antigens may be tran
225 ric form of the toxin, suggesting that human B cells recognize epitopes on the dimerized form of LukA
228 34-expressing clones are common in the naive B cell repertoire but are rarely found in IgG memory B c
231 e have demonstrated that the kinetics of the B cell response are similar for all four FMDV serotypes
233 nt resulted in suppression of virus-specific B cell responses by inhibiting proliferation of germinal
239 mechanisms of antibody production in memory B cell responses.IgE is an important mediator of protect
243 alysis of B6 Ifnb(+/+) versus B6 Ifnb(--) T1 B cells revealed heterogeneous expression of Ifnb in wil
245 protective or deleterious effects on loss of B cell self-tolerance in vivo, we depleted neutrophils a
246 assenger allele system to assay, in mouse GC B cells, sequence-intrinsic SHM-targeting rates of nucle
248 ned a model of specific antibody deficiency, B cell-specific CD79a-Cre x XBP1 (X-box binding protein-
251 rtial deletion at the transitional to mature B cell stage, but become Env(-) upon receptor editing.
253 tometry analysis of the splenic transitional B cell subsets demonstrated that MZ B cell development w
254 ctions with regard to dynamics of the memory B cell subsets point to their role in the pathogenesis o
255 nerated IgE(+) cells, the capacity of tonsil B-cell subsets to generate IgE(+) PCs and the class swit
257 ng a multivalent immunogen, rare VRC01-class B cells successfully competed in germinal centers (GC),
259 oxin-elicited suppression of early B and pro-B cells, suggesting a role of AHR in regulating B lympho
262 Delivery of neurotransmitters across the T-B-cell synapse may be advantageous in the face of infect
265 ), MRD detection method, phenotype/genotype (B cell, T cell, Philadelphia chromosome), and EFS and OS
267 entify critical immunoregulatory circuits in B cells that may be targeted to promote long-lived humor
269 ystems of infected hosts to recall of memory B cells that recognized the lateral patch, the principal
271 rom human immature dendritic cells and naive B cells to assess the expression of CD40-downstream gene
276 strategy to reliably identify blood IgG4(+) B cells to study their cellular and molecular characteri
277 cking of FDC secretion of IFN-alpha restored B cell tolerance and reduced the amount of GCs and patho
281 eveal an important role for RUNX3/CBF during B cell transformation and EBV latency that was hitherto
283 arrested B-lymphopoiesis at the pro-B to pre-B-cell transition and, contrary to their proposed domina
284 icantly increases CD20 levels in established B-cell tumor cell lines and primary malignant cells.
285 crete proportion of infiltrating T cells and B cells underwent proliferation within the pituitary par
286 differentiation of sorted LPS-stimulated MZ B cells was impaired, and aged bumble mice were unable t
288 antly, very high numbers of antigen-specific B cells were detected in local genital draining lymph no
289 ed that frequencies of class-switched memory B cells were increased in the patients, whereas frequenc
292 genes in immature dendritic cells and naive B cells were significantly enriched in synovial tissues
293 diating xenobiotic toxicity, is expressed in B cells, which are known targets for environmental pollu
295 The chemokine CXCL13 recruits both Tfh and B cells, which is essential for the homing of Tfh cells
296 lly, CpG increased the number of circulating B cells, which produced elevated amounts of tumor necros
297 lymphoid tissues, clusters of proliferating B cells with a GC-like phenotype can be generated in the
300 lin light chain editing occurred, generating B cells with up-regulated Nod1, including follicular and
301 protein 3 (EBI3) mRNAs were detected only in B cells, with a trend toward a lower level among patient
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