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1 PCs with repopulation from clonally related memory B cells.
2 i.e., activated memory cells and tissue-like memory B cells.
3 IV increased frequencies of plasmablasts and memory B cells.
4 ) PBs, and CD20(+)CD27(+)CD38(lo/int)CD43(-) memory B cells.
5 27(+) B cells--are post-germinal center (GC) memory B cells.
6 PPE1 enhanced IgE also in human memory B cells.
7 dependent on protection by pathogen-specific memory B cells.
8 for the long-term maintenance of Ag-specific memory B cells.
9 n and the development of active autophagy in memory B cells.
10 e in both the proportion and number of CD27+ memory B cells.
11 allows age-dependent accumulation of resting memory B cells.
12 body responses, long-lived plasma cells, and memory B cells.
13 ace over time after the initial formation of memory B cells.
14 re CD5(+), IgM(+) memory, and class-switched memory B cells.
15 ory receptor expressed by a subpopulation of memory B cells.
16 to naive B cells and to IgM-only and IgG(+) memory B cells.
17 T cell-independent CD27(-)IgA(+) circulating memory B cells.
18 and associated with an increased fraction of memory B cells.
19 a cells, but not circulating plasmablasts or memory B cells.
20 differentiation to produce plasma cells and memory B cells.
21 ndent accumulation of class-switched resting memory B cells.
22 eks, facilitating Ag presentation to cognate memory B cells.
23 ression; and the ability to generate optimal memory B cells.
24 ed and T regulatory cells and also naive and memory B cells.
25 artment of IgM(+)(IgD(+)) and class-switched memory B cells.
26 cells, antibody-secreting plasma cells, and memory B cells.
27 reting cells, as well as germinal center and memory B cells.
28 clones, especially among non-class-switched memory B cells.
29 matic hypermutation, and differentiated into memory B cells.
30 ciated with reduced frequency of circulating memory B-cells.
31 anisms, unmasking CD22 relative to naive and memory B-cells.
32 apy), decreased percentages of IgM+CD21-/low memory B cells (35.7% +/- 6.1% before therapy vs 14.9% +
34 nd avidities of IgG and lower frequencies of memory B cells against Expanded Program on Immunization
36 isolation and characterization of AHAs from memory B cells, although anti-hinge-reactive B cells wer
37 ively associated with proportions of CD27(+) memory B cells among farmers' children and inversely rel
38 cquired phenotypes of atypical and classical memory B cells and 9G4(+) IgG contained equivalent numbe
39 nal center reaction, and they developed into memory B cells and Ab-secreting cells that were capable
41 atients with severely reduced class-switched memory B cells and an elevated level of CD21(lo) B cells
42 ers and found to have reduced frequencies of memory B cells and antigen-specific antibody-secreting c
43 al profile was equally dissimilar to healthy memory B cells and circulating B cells likely due increa
44 numbers were normal, but the proportions of memory B cells and EBV-specific effector memory CD8(+) T
45 rial, we sorted hemagglutinin cross-reactive memory B cells and identified three antibody classes, ea
46 allergen exposures that recurrently activate memory B cells and identify these as a therapeutic targe
48 donors) MHC-II expression as class-switched memory B cells and intermediate costimulatory molecule e
49 e associated with a significant reduction in memory B cells and no evidence of circulating antibody-s
50 show that the Env-specific circulating IgG, memory B cells and plasma cells displayed similar kineti
51 r affinity maturation and the development of memory B cells and plasma cells, while regulatory CD4(+)
53 ons of activated mature B cells, tissue-like memory B cells and plasmablasts, and low proportions of
54 human B cells, with a focus on HIV-specific memory B cells and plasmablasts/cells that are responsib
56 lele induced haploinsufficiency in naive and memory B cells and recapitulated abnormal immunologic fe
59 correlation between numbers of IgM+CD21-/low memory B cells and T-regulatory cells (P = .03), and pos
60 t they represent germinal center-derived IgM memory B cells and that IgM memory and MZ B cells consti
61 o postinfection the proportion of IgG2a/c(+) memory B cells and the systemic levels of lymphocytic ch
63 y selection thresholds on cells entering the memory B-cell and plasma cell pools, as exemplified by t
64 were measured in the blood (plasmablasts and memory B cells) and in the bone marrow (plasma cells).
65 or induction of cross-reactive plasmablasts, memory B cells, and cytokine-secreting CD4(+) and CD8(+)
66 ctivated B cells and circulating tissue-like memory B cells, and expansion of the B regulatory cells
67 ed frequencies of plasmablasts, PLA-specific memory B cells, and IL-10-secreting CD73(-) CD25(+) CD71
68 cells, in contrast to mature naive B cells, memory B cells, and plasmablasts, were hypersensitive to
69 n affects allospecific and pathogen-specific memory B cells, and reason that these investigations can
72 activated memory and CD27(+)CD21(+) resting memory B cells, and subphenotypes with novel patterns of
73 numbers of naive CD8(+) T cells and switched memory B cells, and TH1/TH2 cytokine imbalance improved
75 ed rare affinity-matured human NANP-reactive memory B cell antibodies elicited by natural Pf exposure
76 After purification, antigen-specific mouse memory B cells are first single-cell-sorted by fluoresce
77 and CD8(+) T lymphocytes as well as switched memory B cells are mostly targeted by the injection-only
79 cades downstream of the BCR are blocked, and memory B cells are temporarily silenced, preventing them
80 this B-cell subset, this establishes IgM(+) memory B cells as a general target of lymphoproliferatio
82 gative patients, P=0.0008) at the expense of memory B cells, as were BAFF serum levels (1,651 +/- 1,2
84 ugh cognate interactions between T cells and memory B cells (B(mem)) are essential for the secondary
87 -IL-7 improved the percentages of long-lived memory B cells (Bmem) in the draining LNs and plasma cel
88 of serotype-specific plasma cells (PCs) and memory B-cells (Bmems) as potential predictors of long-t
89 milarity of IgM(+)(IgD(+))CD27(+) and IgG(+) memory B cells but also pointed at distinct functional c
90 s not critical for the initial generation of memory B cells but is required for their long-term persi
93 stent high-affinity functional Ab titers and memory B cells, but how it really shapes the Ag-specific
94 indicate that naturally acquired PS-specific memory B cells, but not levels of circulating IgG at tim
95 In contrast, SHM reduced the longevity of memory B cells by creating polyreactive specificities th
96 reveals a functional plasticity of human IgM memory B cells by showing their propensity to undergo se
97 ptosis could be transferred to healthy donor memory B-cells by co-culturing these cells with plasma f
98 istic of plasmablasts, and transitioned into memory B cells (CD38(-)CD27(+)) at the early convalescen
99 numbers of T-regulatory cells, IgM+CD21-/low-memory B cells, CD4+CXCR5+ interleukin 21+ cells, and T-
100 production and find that two subsets of IgG1 memory B cells, CD80(+)CD73(+) and CD80(-)CD73(-), contr
101 In conclusion, this study substantiates memory B-cell characteristics of human IgM(+)IgD(+)CD27(
104 roduce amazingly large, complex, and diverse memory B-cell clones, equipping the human immune system
106 contrast, the interrogation of the quiescent memory B cell compartment is technically more challengin
107 ition and intraclonal diversity of the human memory B-cell compartment and the relationship between m
109 xpanded clones, demonstrating that the human memory B-cell compartment is characterized by many, ofte
111 ) B cells appeared in classical and atypical memory B cell compartments in African children and adult
114 ) transitional and CD19(+)CD24(-)CD38(-) new memory B-cell counts were higher in patients with AD ver
115 CVID) present with severely reduced switched memory B-cell counts, and some display an increase of CD
118 lop carriage, the number of circulating 6BPS memory B cells decreased and the number of 6BPS plasma c
120 .277] 10 cells/L) and selective depletion of memory B cells despite normal B cell survival ligand con
121 mote aberrant GC responses with autoreactive memory B cell development and plasma cell-derived autoan
123 In this study, we show that newly generated memory B cells do not display active autophagy but are c
124 (+)38(hi) B cells or PBs, but differ in that memory B cells do not express Ab secretion-related genes
125 ed by loss of naive B cells, loss of resting memory B cells due to their redistribution to the gut, i
132 nses, as neither long-lived plasma cells nor memory B cells form for months after infection, and nons
133 centers (GCs) are required for high-affinity memory B cell formation; however, the signals that commi
136 nes that augment B-cell responses and higher memory B-cell frequencies correlate with stronger respon
137 we observed decreased frequencies of SHM in memory B cells from AD-AID patients and AID+/- subjects,
145 ter re-infection, somatically mutated IgM(+) memory B cells function as first responders by rapidly d
146 llicular helper (pTfh) cells correlated with memory B-cell function and influenza A(H1N1) antibody ti
147 ect memory B cells, leading to inhibition of memory B-cell function and persistent HCV infection in H
148 linked immunosorbent assay, and frequency of memory B cells, functional T-cell responses, and antigen
151 ing clear, as in some patients, HLA-specific memory B cells have been shown to be present in the abse
152 ental models are providing new insights into memory B cell heterogeneity with respect to their phenot
153 ed single B cell analysis to interrogate the memory B cell Ig repertoires from two rhesus macaques af
154 Frequencies of AF DENV(+) class-switched memory B cells (IgD(-)CD27(+) CD19(+) cells) reached up
155 of total memory (CD27(+)) and class-switched memory B cells (IgM(-)) were significantly reduced in pa
156 cells and total and NV-specific IgA and IgG memory B cells) immune responses following infection.
159 investigate the function of subsets of IgG1 memory B cells in IgE production and find that two subse
161 CD27(+)) and resting (CD19(+)CD27(+)CD21(+)) memory B cells in parallel to increased naive (CD19(+)CD
162 cell tetramer to define Plasmodium-specific memory B cells in parasite-infected mice and demonstrate
164 cell subsets and frequencies of Ag-specific memory B cells in peripheral blood from HIV-infected chi
165 a higher number of circulating Env-specific memory B cells in peripheral blood of AGMs than in the b
166 cross-reactive antibodies derived from blood memory B cells in RMs as observed in the HVTN 505 vaccin
167 increases in the numbers of antigen-specific memory B cells in spleens and plasma cells in bone marro
171 ll dysfunction (defined by loss of total and memory B cells, increased B regulatory cell [Breg] count
172 ver, only delayed reconstitution of switched memory B cells, independent of immunosuppressive treatme
173 provide strong evidence for the existence of memory B-cell-independent, long-lived PCs in humans that
174 -product relationships with CD27(+) switched memory B cells, indicating that they represent germinal
175 expression between naive and class-switched memory B cells, indicating their potential to induce (pr
176 heories that reactivation/differentiation of memory B cells into plasma cells is required to sustain
177 gE and the clonal selection of high affinity memory B cells into the plasma cell fate, our findings p
180 oth infants and toddlers upon infection, and memory B cells isolated from individuals who previously
181 ptor B7.2 enabled lymphotropic HCV to infect memory B cells, leading to inhibition of memory B-cell f
184 disease relevant genes, as for instance the memory-B cell marker CD27 and PTPRC genes, providing us
186 similar B-blasts can differentiate to become memory B cells (MBC), in which EBV persistence is establ
191 ate into antibody-secreting cells (ASCs) and memory B cells (MBCs) after infection or vaccination.
192 pic overexpression of FOXP1 in primary human memory B cells (MBCs) and B-cell lines, combined with ch
193 the signals that control differentiation of memory B cells (MBCs) and long-lived plasma cells (LLPCs
194 associated with a large increase in atypical memory B cells (MBCs) that resemble B cells expanded in
196 of Ab immunity, long-lived plasma cells and memory B cells (MBCs), is remarkably inefficient, requir
201 We cloned one of these antibodies, 3H3, from memory B cells of a healthy individual using a hybridoma
202 clones were seen predominantly among IgM(+) memory B cells of all HCV-infected patients analyzed.
203 The demonstration of gp41 immunodominance in memory B cells of both adult and neonatal RMs indicated
204 (mAbs) specific for LASV glycoproteins from memory B cells of Lassa fever survivors from West Africa
208 OR] = 1.34, 95% CI 1.14-1.57; p < 0.001) and memory B cells (OR = 1.18, 95% CI 1.0-1.39; p = 0.04) we
210 01), but higher proportions of IgM+CD21-/low memory B cells (P < .05), CD4+IFNgamma+ cells (P < .01),
211 subsets, including a significant decrease in memory B cells, particularly of marginal zone (MZ) B cel
212 ew sex differences were seen in Env-specific memory B cell, plasmablast, or plasma cell frequencies i
213 rther suggest that establishing an optimized memory B cell pool should be an aim of 'universal' influ
216 samples from the same study, we investigated memory B cell population dynamics in blood, bone marrow,
219 ic, and PspC-specific IgG and IgA plasma and memory B-cell populations before and 7, 14, and 35 days
220 i and compare the proportion of Env-specific memory B-cell populations to that of HIV-infected humans
222 ll differentiation, whereas activated IgG(+) memory B cells preferentially showed a plasma cell (PC)
225 ntage for donor-derived T cells and switched memory B cells promoted restoration of cellular and humo
226 e binding site of CD22 relative to naive and memory B-cells, promoting recognition of trans ligands.
227 w production of antibody-secreting cells and memory B cells recognizing that strain upon revaccinatio
235 erotype-specific IgG, opsonophagocytosis, or memory B-cell response at either time point between chil
237 -cell compartment in terms of frequencies of memory B cells, response to in vitro stimulation, and ma
240 fundamental questions about antigen-specific memory B cell responses, as well as for characterizing a
242 on the mechanisms of antibody production in memory B cell responses.IgE is an important mediator of
243 onophagocytosis for 8 vaccine serotypes, and memory B-cell responses for 18 serotypes before and afte
245 by a hemagglutination inhibition assay, and memory B-cell responses were evaluated by an enzyme-link
247 e did result in decreased TACI expression on memory B cells, resulting in impaired activation and ant
248 pothesized that the disappearance of CD27(+) memory B-cells results from enhanced sensitivity to apop
249 01 human V region expressed in vivo by human memory B cells revealed that the focus of mutations in c
250 ing-based repertoire analysis of circulating memory B cells reveals evidence for convergent selection
254 g of the BCR from E2-specific class-switched memory B cells sorted from two independent participants
255 r 2 virus NAb responses, we performed single memory B cell sorting from the peripheral blood of a rhe
256 on, followed by the contraction, of a single memory B cell SPADE cluster was positively correlated wi
258 T cells, spontaneous Ab secreting cells and memory B cells specific to influenza hemagglutinin were
260 ic infections with regard to dynamics of the memory B cell subsets point to their role in the pathoge
261 te total and mature B cell recovery, whereas memory B cell subsets remained significantly depleted.
262 e highly similar to each other and to IgG(+) memory B cell subsets, with typical upregulation of acti
263 ell compartment and the relationship between memory B-cell subsets is still limited, although these a
266 elicited a higher frequency of gp41-reactive memory B cells than gp120-memory B cells in adult and ne
267 xpression, B-1 cells align more closely with memory B cells than with 20(+)38(hi) B cells or PBs, but
268 yet little is known about the properties of memory B cells that are central to the recall alloantibo
270 n of virus-specific B lymphocytes, including memory B cells that differentiate into ASC soon after co
271 zing antibody titers have expanded clones of memory B cells that express the same immunoglobulin VH3-
274 mmune systems of infected hosts to recall of memory B cells that recognized the lateral patch, the pr
275 is conferred by allergen-specific long-lived memory B cells that replenish the IgE(+) PC compartment.
276 doses of vaccine, the majority of donors had memory B cells that secreted IgGs specific for H7 HA, wi
277 tem-directed bnAb, 3I14, isolated from human memory B cells, that utilizes a heavy chain encoded by t
278 are able to activate and expand Ag-specific memory B cells; these cultured cells are highly effectiv
279 an already primed immune system to diversify memory B cells to recognize closely related, but antigen
281 +)CD27(+) B cells in that they share typical memory B-cell transcription patterns with IgG(+) post-GC
284 lescence, only IgG (and no IgA) RSV-specific memory B cells were detectable in peripheral blood.
286 revealed that frequencies of class-switched memory B cells were increased in the patients, whereas f
287 lly activated CD27(+) memory and nonswitched memory B cells were observed in patients with AD (P < .0
290 ed cytotoxicity and degranulation, levels of memory B cells were reduced, and serum IgG4 levels were
291 ivated homed to the lamina propria) and CD44 memory B cells, whereas PN-BBS assimilated chow levels.
292 s, we found that, in contrast with naive and memory B cells, which gathered antigen toward the synaps
293 hancing BCR signal strength permitted IgE(+) memory B cells-which essentially do not exist under norm
294 e and the severe reduction in class-switched memory B cells, while gathering longitudinal laboratory
295 tent infection within a subset of its host's memory B cells, while lytic EBV replication takes place
296 immunoglobulin heavy chains from circulating memory B cells with 2x250 paired-end sequencing on the I
297 were shown to harbor H-2K(d)-specific IgG(+) memory B cells with a post-germinal center phenotype (CD
298 s induced a relative decrease in circulating memory B cells with concomitant expansion of circulating
299 cursor, transitional T3, and PDL-2(+)CD80(+) memory B cells, with significantly elevated CD69 and CD8
300 rated via class-switch recombination in IgG1 memory B cells without additional somatic hypermutation.
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