コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 revealed that they were enriched in a CD9(+) B cell subset.
2 e activation and temporary expansion of this B cell subset.
3 strong orientation toward the marginal zone B cell subset.
4 ting in a reduction in the size of the naive B cell subset.
5 ecognized CD5(+)CD27(+) post-germinal center B cell subset.
6 cells, suggesting an important role for this B cell subset.
7 L) are highly suggestive that they are a new B cell subset.
8 organ cellularity, most prominent among the B-cell subset.
9 is associated with the apoptosis of multiple B cell subsets.
10 7(-)IgM(+), CD27(+)IgM(+), and CD27(+)IgG(+) B cell subsets.
11 inders from the follicular and marginal zone B cell subsets.
12 rongest proliferative response of all memory B cell subsets.
13 ing a chemotactic effect of eotaxin on these B cell subsets.
14 turation status of human CD21/CD24 nonmemory B cell subsets.
15 sequent changes in proportions of individual B cell subsets.
16 are expressed at different levels by various B cell subsets.
17 elatively constant level throughout numerous B cell subsets.
18 transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets.
19 4(high)CD21(low)) and T2 (CD24(high)CD21(+)) B cell subsets.
20 duced the highest c-Rel protein levels among B cell subsets.
21 ng fungal load that was independent of T and B cell subsets.
22 vely selected into the marginal zone and B-1 B cell subsets.
23 on sites in Ab V regions of naive and memory B cell subsets.
24 shape the epigenome of expanded SLE effector B cell subsets.
25 etermine how CD19 affects CNS recruitment of B cell subsets.
26 mainly derive from T cell-independent innate B cell subsets.
27 hat seen in old follicular and marginal zone B cell subsets.
28 ies have mainly focused on B1 and follicular B cell subsets.
29 B1 cell BCR signaling is distinct from other B cell subsets.
30 related genes and the relative expansions of B cell subsets.
31 the four main human IgM(+) and IgG(+) memory B-cell subsets.
32 ression of IL-10 and are enriched in various B-cell subsets.
33 ing plasma cells and 2 IgE-expressing memory B-cell subsets.
34 uppressive capacity of both memory and naive B-cell subsets.
35 n and internalization of cross-linked BCR in B-cell subsets.
36 ancreatic and splenic suppressive FasL(high) B-cell subsets.
37 regulated signatures compared with the other B-cell subsets.
38 g in vivo BAFF dependence of these 2 CD27(+) B-cell subsets.
39 ular kinases identified activation status of B-cell subsets.
40 4(+) T-cell reduction, and changes in T- and B-cell subsets.
41 to determine the frequencies of circulating B-cell subsets.
42 eceptor expression in newly formed and naive B-cell subsets.
43 lular immunity, involving various T-cell and B-cell subsets.
44 WM patients in relation to normal plasma and B-cell subsets.
45 ptor after CD40 engagement compared to other B-cell subsets.
48 examined the dynamics of BAFF induction and B cell subset activation and composition, to investigate
49 both the CD27(+) memory population and naive B cell subset after only a brief stimulation in vitro.
51 ndard immunophenotyping of circulating human B cell subsets, an in vitro CFSE dilution assay was used
52 dies to polysaccharide antigens by the human B-cell subset analog to murine B-1 cells was reported in
54 signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity
55 2B low/neg cells in the CD27(+)IgD(-) memory B cell subset and that these changes are associated with
56 s associated with normalization of activated B cell subsets and allows age-dependent accumulation of
57 ress the highest levels of FcgammaRIIb among B cell subsets and are highly susceptible to FcgammaRIIb
60 surface expression of BTLA on various human B cell subsets and confirm its ability to attenuate B ce
61 (T1) stage and leads to a decrease in mature B cell subsets and deficits in T cell-dependent antibody
63 develop normal B1 and B2 immature and mature B cell subsets and have normal levels of naive serum Abs
65 ht the phenotypic heterogeneity of innate B1 B cell subsets and of their possible fates in a relevant
66 and activated NK cells, differentiated T and B cell subsets and proinflammatory monocytes, suggesting
67 isolation of antibodies from all peripheral B cell subsets and revealed the anti-BK virus antibody r
68 ar to a previously described FCRL4(+) memory B-cell subset and to an "exhausted," anergic CD21(low) m
69 ns and thymi from 3-week-old pups for T- and B-cell subsets and epithelial cells did not show any sig
70 identified differential effects of different B-cell subsets and helped to clarify the still poorly un
71 n of anti-PS antibodies or anemia with other B-cell subsets and no association of other antibody spec
72 authors studied by flow cytometry peripheral B-cell subsets and serum levels of BAFF, the main homeos
73 intain stable relative levels of circulating B cell subsets, and a potential mechanism for viral rese
74 atory biomarkers, the proportions of various B cell subsets, and fetal priming to tetanus vaccination
75 ntly up-regulated on monocytes, neutrophils, B cell subsets, and plasma cells in multiple murine mode
80 replasma and plasma B cells, newly developed B-cell subsets, and their apoptosis was performed 30-60
83 peripheral B cell compartment, although all B cell subsets are present in relatively normal ratios.
84 asmablast B-cell development, and that these B-cell subsets are dependent on T-cell-derived signals t
85 g cells resided mainly in the CD19(+) CD5(-) B cell subset, as assessed by enzyme-linked immunosorben
88 tic stem cell (HSC) gives rise to all of the B-cell subsets [B-1a, B-1b, B-2, and marginal zone (MZ)
89 IL-10-producing CD1d(high)CD5(+) regulatory B cell subset (B10 cells) have been identified during th
90 epleted, particularly a rare IL-10-producing B cell subset (B10 cells) known to regulate inflammation
91 a rare IL-10-producing CD1dhiCD5+ regulatory B cell subset (B10 cells), since the adoptive transfer o
93 Flow cytometry was used to analyze CD19(+) B cell subsets based on the expression of CD24 and CD38.
94 aluated phenotypic definition of circulating B-cell subsets before and after standard of care and B-c
95 trols, but there was no difference in memory B cells subsets between controls and splenectomized subj
97 ll compartment with a normal distribution of B-cell subsets both in bone marrow and the periphery, sh
98 t change other previously defined regulatory B-cell subsets (Breg), including CD5CD1d Breg or express
99 antibody results in significant depletion of B cell subsets but does not affect anti-peanut IgE level
100 shared with other mature perinatal or adult B cell subsets but were either unique or variably shared
101 onfer regulatory functions to various mature B-cell subsets but immature B-cell progenitors endowed w
102 L-10 production was not confined to a single B-cell subset, but enriched in both the CD24(hi)CD27(+)
103 erely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be l
104 Thy-1 autoreactive (ATA) BCR cells in the B1 B cell subset by transgenic expression yielded spontaneo
106 on at the protein level was confirmed in UCB B cell subsets by intracellular staining and flow cytome
107 cent studies in Hep-2 cells; quantitation of B-cell subsets by means of flow cytometry; assessments o
111 B cells in three circulating naive or memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+
112 , depletion of the prominent IL-10-producing B-cell subset, CD1d(hi) cells, resulted in less IL-10(+)
113 characterized a distinct, late transitional B cell subset, CD21(int) transitional 2 (T2) B cells.
114 longitudinal study of its kind, we measured B cell subset composition, as well as PfEMP1-specific Ab
117 ormed high-throughput VH sequencing of human B cell subsets defined by IgD and CD27 expression: IgD(+
118 tometry analysis of the splenic transitional B cell subsets demonstrated that MZ B cell development w
119 tuted with T2-MZP B cells but not with other B cell subsets displayed accelerated tumor growth, demon
122 to analyze the potential association between B-cell subsets distribution and anti-HLA antibodies befo
123 e study aimed to verify the relation between B cell subsets' distribution and liver disease progressi
126 on signals driving CNS migration of distinct B cell subsets during neuroinflammatory insults is criti
127 egulating differentiation and maintenance of B-cell subsets during an immune response is unclear.
128 nse to this virus is contributed by multiple B cell subsets, each generating qualitatively distinct r
129 for the existence of different transitional B-cell subsets, each displaying unique phenotypic and re
132 ntrast, ATA B-CLL did not develop from other B cell subsets, even when the identical ATA BCR was expr
133 ction in each of the major mature peripheral B-cell subsets, exerting the greatest impact on marginal
135 in which the major immunoglobulin M (IgM(+)) B-cell subset expresses green fluorescence protein (GFP)
140 Immature transitional and mature activated B cell subset frequencies were increased in HCV-infected
141 re activated, tissue-like memory, and plasma B cell subset frequencies, cell cycling, and intrinsic a
143 ne cells, we performed RNA-seq in T cell and B cell subsets from either healthy donors or patients wi
144 criptome analyses of CLL and the main normal B cell subsets from human blood and spleen revealed that
147 subsets, including a newly defined effector B cell subset, from subjects with SLE and healthy contro
152 es that altered distribution of transitional B-cell subsets highlights different regulatory defects i
155 ciated with an accumulation of heterogeneous B cell subsets; however, their influence on viral load a
156 of two major, functionally distinct, mature B cell subsets, i.e., follicular mature (FM) and margina
160 s, the proportions of naive and memory T and B cell subsets in A-T patients did not vary in relation
162 the characterization of autoantigen-specific B cell subsets in different models of autoimmunity and,
163 hat different Borrelia can activate the same B cell subsets in distinct ways and they each elicit a c
164 g cytokine-producing regulatory and effector B cell subsets in health and disease and discuss how fut
165 ow that changes in P. falciparum Ag-specific B cell subsets in HIV-infected individuals mirror those
167 Additionally, the monitoring of individual B cell subsets in patients may lead to the discovery of
168 well as the proportion and numbers of major B cell subsets in peripheral lymphoid organs, was unaffe
169 serologic activity and reduce BLyS-dependent B cell subsets in serologically and clinically active SL
170 a B cells are greatly expanded into effector B cell subsets in some autoimmune mice, thus indicating
172 e findings demonstrate the plasticity of the B cell subsets in virus-infected hosts and show for the
175 ound that IgT(+) B cells represent the major B-cell subset in the skin epidermis and that IgT is main
176 linked immunospot assay (ELISPOT) to examine B-cell subsets in 59 subjects, including 28 with PBC, 13
177 We analyzed the reconstitution kinetics of B-cell subsets in adult leukemic patients within 6 month
178 t in our understanding of the role of T- and B-cell subsets in atherosclerosis and addresses the role
179 eriphery, (ii) expansion of CD80+ and CD62L- B-cell subsets in BM and the periphery, and (iii) a sign
182 d heavy-chain genes from immature and mature B-cell subsets in mice, we demonstrate a striking gradie
183 mpaired humoral response, we assessed memory B-cell subsets in paired samples collected before and af
184 We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of
185 ic differentiation is skewed toward specific B-cell subsets in the embryo are unanswered questions, b
186 ant early depletion of both naive and memory B-cell subsets in the peripheral blood, with differentia
188 ore, the altered numbers of naive and memory B-cell subsets in these animals corresponded with increa
190 profiles and transcriptomes from five human B cell subsets, including a newly defined effector B cel
192 rations were associated with an imbalance in B-cell subsets, including a significant decrease in memo
193 with CD19-Cre and found that all peripheral B-cell subsets, including B1 B cells, require YY1 for th
194 inct DNA methylation signatures specific for B-cell subsets, including memory B cells (MBCs) and plas
196 rthermore, B2 cells, in the absence of other B-cell subsets, increase splenic regulatory T-cell popul
197 dicated by a marked disruption of peripheral B cell subsets, increased levels of PD-1 expression, and
198 of ART restored the typical distribution of B cell subsets, increasing the proportion of naive B cel
199 variably designed to deplete specific T and B cell subsets, interrupt receptor-ligand interactions,
200 Thus, by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote optimal T-indepe
204 partment and the relationship between memory B-cell subsets is still limited, although these are cent
206 ocystis challenge, suggesting that different B cell subsets may be responsible for the generation of
207 The reported microarray analysis of human B cell subsets may now be used to delineate B cell defec
208 und humoral immunodeficiency and lack mature B cell subsets, mirroring deficiency of the cytokine B c
210 munity, neither the initiating event nor the B cell subset necessary for WP formation has been identi
211 for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus.
212 boost of 2 clonally and functionally related B-cell subsets of short-lived IgE(+) plasmablasts and Ig
216 n), proportion of Bm2 cells but not of other B-cell subsets or BAFF levels was independently associat
217 e global quantitative recovery of T-cell and B-cell subsets or in global T-cell and B-cell function.
218 e or particulation, selective recruitment of B cell subsets, or activation and recruitment of Pn prot
220 B cells play in establishing, and the roles B cell subsets play in maintaining lifelong anti-peanut
221 ctions with regard to dynamics of the memory B cell subsets point to their role in the pathogenesis o
223 n leads to an abnormally expanded CD5(+) B1a B-cell subset (present as early as 4 days after birth),
224 re enriched in the IgM(high)CD5(+)CD1d(high) B cell subset previously reported to contain a higher fr
226 are still unknown, we studied five precursor B cell subsets (ProB, PreBI, PreBII large, PreBII small,
228 st an important role of BAFF in facilitating B cell subset proliferation and redistribution as a cons
229 rine B-1b and primate IgM(+)CD27(+) "memory" B cell subsets proposed to produce TI-2 Ab responses may
234 We studied peripheral B- and T-cell subsets, B-cell subset replication history, somatic hypermutation
235 mory T and B cells may limit MS, rapid CD19+ B-cell subset repopulation in the absence of effective T
236 low cytometric analysis of tetramer-reactive B cell subsets revealed a significantly higher frequency
238 In NOD, btk deficiency mirrors changes in B cell subsets seen in other strains, but also improves
239 memory B cells and the activation of sorted B cell subsets shows that GA-dependent increased Breg ce
241 infection, a state of activation results in B cell subset skewing that is likely the result of alter
242 Second, we examined colonization by EBV of B-cell subsets sorted from a unique collection of IM ton
243 on, the peripheral CD19CD24CD38 transitional B cell subset strongly declined, regardless of the subse
244 vels of eotaxin receptor CCR3 than the other B cell subsets, suggesting a chemotactic effect of eotax
245 s impaired TLR-induced proliferation of this B-cell subset, suggesting a means by which loss of this
246 identified IL-10-competent CD1d(high)CD5(+) B cell subset termed B10 cells that represents 1-3% of a
248 Marginal zone B cells (MZB) are a mature B cell subset that rapidly respond to blood-borne pathog
249 al center fate, and we identified a CD11c(+) B cell subset that was not capable of producing IL-10 ev
250 erstanding of the abundance and phenotype of B cell subsets that are induced or perturbed by exogenou
255 in this issue of Blood, identified a pre-pro-B-cell subset that marks the earliest stages of B-cell l
256 and genetic approaches, we discovered a new B-cell subset that, upon adoptive transfer into B cell-d
257 cted individuals, focusing on the skewing of B-cell subsets that circulate in the peripheral blood an
259 by the functional balance between different B-cell subsets that may be generated by this therapeutic
260 epleting antibody rituximab, the size of all B cell subsets, the T1/T2-ratio, and the cyroglobulin le
261 pite sharing some features with other mature B-cell subsets, they are refractory to BCR and CD40 stim
262 clones in MC and lymphomas derive from this B-cell subset, this establishes IgM(+) memory B cells as
264 tics of LANA/EBNA-1 expression in individual B-cell subsets throughout a course of infection has not
265 ll lymphomas, indicating sensitivity of this B cell subset to transformation caused by p53 deficiency
267 how viral gene products function in specific B cell subsets to regulate this process is incomplete.
269 nerated IgE(+) cells, the capacity of tonsil B-cell subsets to generate IgE(+) PCs and the class swit
271 mononuclear cells were quantified for T and B cell subsets using flow cytometry, and serum cytokine
272 skewing (lower T1/T2-ratio) of the immature B cell subset was noted in MC patients, suggesting that
273 ution of HIV-specific responses among memory B cell subsets was corroborated by transcriptional analy
277 Consistent with an increased number of these B cell subsets, we detected elevated levels of IgG3 natu
279 n those SLE patients occurred throughout all B cell subsets, we hypothesized that ARID3a expression i
280 whole-genome bisulfite sequencing of normal B cell subsets, we observed broad epigenetic programming
281 ther B-cell lymphomas, cHL lines, and normal B-cell subsets, we show that they differ extensively fro
287 phenotype, specificity, and functionality of B-cell subsets were studied in a cohort of pregnant wome
288 oper development and function of the various B cell subsets while counteracting lymphomagenesis.
289 ional B cells, including a late transitional B cell subset with a phenotype intermediate between T2 a
291 EBV infection induced redistribution between B cell subsets with enrichment of IgD(+)CD27(+) cells (c
296 y similar to each other and to IgG(+) memory B cell subsets, with typical upregulation of activation
297 plasmablasts and plasma cells than in other B-cell subsets, with higher levels in patients with SLE
298 Chemokine-dependent localization of specific B cell subsets within the immune microarchitecture is es
299 t the pathologic cytokine-producing effector B cell subsets without impacting the protective regulato
300 he maturation and functionality of all major B cell subsets, yet the molecular players in these signa