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1 or using small bioactive molecules to direct germinal activity in the SVZ, which has therapeutic pote
5 s capable of measuring total and Ag-specific germinal center (GC) B cell and follicular Th cell respo
6 rated that E2A together with E2-2 controlled germinal center (GC) B cell and plasma cell development.
9 own that type I latency is associated with a germinal center (GC) B cell phenotype, and type III late
10 cells profoundly impaired the acquisition of germinal center (GC) B cell phenotype, plasma cell gener
12 ate IL-21 and IL-17A, which drive pathogenic germinal center (GC) B cell reactions and monocyte-macro
14 lar Th (Tfh) cells orchestrate physiological germinal center (GC) B cell responses, whereas in lupus
16 tly mutated in the activated B cell-like and germinal center (GC) B cell-like subtypes of diffuse lar
17 on of the immunoglobulin (Ig) genes occur in germinal center (GC) B cells and are initiated through d
18 ) TET2 is turned off in normal and malignant germinal center (GC) B cells but expressed in other B ce
21 induced higher proportions of TFH cells and germinal center (GC) B cells following immunization than
22 rates of T follicular helper (Tfh) cells and germinal center (GC) B cells from draining lymph nodes (
25 CL13 recruited follicular helper T (Tfh) and germinal center (GC) B cells, promoted the formation of
26 t arise from the malignant transformation of germinal center (GC) B cells, underscoring the importanc
32 d that levels of this molecule are higher in germinal center (GC) B-cell DLBCL (GCB-DLBCL) compared w
34 ics analysis data have implicated YY1 in the germinal center (GC) B-cell transcriptional program.
38 n wild-type (WT) mice and extended them with germinal center (GC) disruption experiments and variable
39 egulators driving B cell differentiation and germinal center (GC) formation by lowering the threshold
41 riptional repressor that is required for the germinal center (GC) reaction and is implicated in lymph
43 t infection depends on the initiation of the germinal center (GC) reaction in secondary lymphoid orga
45 been shown to be critically required for the germinal center (GC) reaction where B cells undergo clas
46 ssed the autoimmune response by reducing the germinal center (GC) reaction, which was associated with
50 he diversity of B cell clones recruited into germinal center (GC) responses is likely to be important
52 Mer-deficient mice (Mer(-/-)) have increased germinal center (GC) responses, T cell activation, and A
55 on is the elimination of viral reservoirs in germinal center (GC) T follicular helper (Tfh) cells.
56 GNA13 is the most frequently mutated gene in germinal center (GC)-derived B-cell lymphomas, including
61 the development of plasmablasts derived from germinal center and extrafollicular sources, we hypothes
62 ulatory (Tfr) cell subset can migrate to the germinal center and inhibit Tfh-mediated B-cell activati
64 ents Ag-specific B cell differentiation into germinal center and memory precursor B cells as well as
65 d that both combinations enhanced lymph node germinal center and T follicular helper cell responses.
66 (CD69 and CD86) on these cells and stronger germinal center B and T cell responses, relative to DV23
67 Id3 expression depleted displayed a block in germinal center B cell maturation, showed reduced number
68 greater impact on changing plasma cells and germinal center B cell populations in females than males
70 stable covalent bond, resulting in enhanced germinal center B cell responses that generated higher a
75 cally enhanced the development of Tfh cells, germinal center B cells and antibody responses against p
76 cacy over soluble glycoprotein in activating germinal center B cells and eliciting tier-2 autologous
78 Enpp1 (-/-) mice generated normal levels of germinal center B cells and plasmablasts in periphery, t
79 to stimulate nitrophenyl-specific lambda(+) germinal center B cells and sequenced the unexpressed ka
81 eased the positive selection of B1 cells and germinal center B cells by self and foreign antigens.
82 l3-/- mice, splenic T and B cells as well as germinal center B cells from Peyer's patches showed mark
84 educed frequency of Peyer's Patches IgG1 and germinal center B cells in addition to small but signifi
86 nalysis of lymphocytes indicated that GL7(+) germinal center B cells were induced at higher levels in
87 the induction of protective IgG antibodies, germinal center B cells, and plasma cells secreting anti
88 genome reorganization from naive B cells to germinal center B cells, centered on a locus control reg
89 IV Env-specific IL-21(+) TFH cells and total germinal center B cells, the size and number of germinal
90 quired for the generation and maintenance of germinal center B cells, which require high glycolytic a
92 essed by FOXP1 in activated B-cell (ABC) and germinal center B-cell (GCB) DLBCL cell lines with aberr
93 howed that BCR signaling differs between the germinal center B-cell (GCB) subtype, which is insensiti
94 ma (DLBCL) subtype from the better prognosis germinal center B-cell (GCB)-DLBCL subtype and is highly
95 to COO (activated B-cell [ABC]-like DLBCL v germinal center B-cell [GCB]-like DLBCL) were observed i
98 es that have prognostic significance, namely germinal center B-cell like (GCB) and activated B-cell l
101 ysis to the 10% of DLBCL patients who have a germinal center B-cell phenotype and coexpress MYC and B
102 s with vaccines toward the goal of enhancing germinal center B-cell responses to favor bNAb B-cell li
105 tain 2 major molecular subtypes; namely, the germinal center B-cell-like (GCB) and the activated B-ce
107 es in previously untreated patients with non-germinal center B-cell-like (non-GCB) diffuse large B-ce
109 lls, but the function of extrafollicular and germinal center CD4(+) T and B interactions in cGVHD pat
110 ivity by direct assessment of GC B cells and germinal center CD4(+) T follicular helper (GC Tfh) cell
111 e mutation frequency was lower than found in germinal center cells after deliberate immunization, sug
112 follicular NKT cells triggers the seeding of germinal center cells and serves as an innate link betwe
115 s cells at governing T follicular helper and germinal center formation after intradermal immunization
117 d proteins in B cells that may contribute to germinal center formation and IgE switching in type 2 im
119 ses: T follicular helper (Tfh) cells support germinal center formation and provide help for affinity
120 or class switch recombination to IgE and for germinal center formation during type 2 immune responses
121 , IL-17 can enhance B cell proliferation and germinal center formation in dry eye disease mice, sugge
123 vation, hypergammaglobulinemia, and enhanced germinal center formation in the absence of organ-specif
125 eleration in the onset of renal disease, SLO germinal center formation, and autoreactive plasma cell
126 differentiation of follicular B cells during germinal center formation, and normal signaling through
127 -ordered trimers enhances B cell activation, germinal center formation, and the elicitation of tier-2
128 specific BTK overexpression show spontaneous germinal center formation, anti-nuclear autoantibodies,
132 typed the NLPHL cell line (DEV) confirming a germinal center immunophenotype, lack of expression of C
133 iency reduces B cell clonal expansion in the germinal center in mice and blocks the proliferation of
134 vel therapeutic targets, and discovered that germinal center kinase (GCK) was extensively activated.
136 henotype (73%), which included expression of germinal center markers (CD75/Bcl-6-positive, CD32-weak/
137 l-defined zonal areas that expressed classic germinal center markers, peanut lectin (agglutinin) and
140 N-gamma production was accompanied by a poor germinal center output, an accumulation of T-box transcr
141 is that disrupt pathways associated with the germinal center reaction (TNFRSF14, IRF8), immune escape
143 ollicular regulatory (Tfr) cells inhibit the germinal center reaction to limit autoantibody productio
144 e rise to B cells capable of entering into a germinal center reaction, and they developed into memory
145 produced by B cells themselves controls the germinal center reaction, plasma cell differentiation, a
150 f tonsils as lymphoid sites for the study of germinal center reactions after vaccination in children.
151 ions demonstrate a role for the Breg cell in germinal center reactions and suggest that deficient act
153 CD4(+) Th (Tfh) cells provide B cell help in germinal center reactions that support class switching,
154 nd NFAT2 in CD4(+) T cells leads to impaired germinal center reactions upon viral infection because o
156 nAb responses were strongly associated with germinal center reactions, as assessed by lymph node fin
160 ed role for MZB cells in controlling the TFH-germinal center response to a cholesterol-rich diet and
162 vels were reduced and, upon viral infection, germinal center responses were defective in TC10-deficie
163 early during development, as well as during germinal center responses, suggesting that T cell-indepe
168 restores their ability to expand and become germinal center T follicular helpers and enhances B cell
175 and is characterized by the accumulation of germinal center-derived malignant B cells engaged in a b
183 urine xenograft models of mantle cell (MCL), germinal-center diffuse large B-cell (GCB-DLBCL), and ac
184 mprints of germinal-center-inexperienced and germinal-center-experienced B cells, and we found that D
185 respectively carrying epigenetic imprints of germinal-center-inexperienced and germinal-center-experi
186 We define the half-lives of antigen-specific germinal centers (23.3 days), IgE(+) and IgG1(+) PCs (60
187 mune response, including in the formation of germinal centers (GC) and the development and maturation
188 et of T follicular helper cells (TFH) within germinal centers (GC) is highly permissive to HIV-1.
189 sis that T follicular helper (Tfh) cells and germinal centers (GC) play a critical role in the abilit
190 VRC01-class B cells successfully competed in germinal centers (GC), underwent extensive somatic hyper
193 f the secondary lymphoid structures known as germinal centers (GCs) and the environmental and signali
194 ypermutation, and affinity maturation within germinal centers (GCs) are required for high-affinity me
197 evalent in women and associates with ectopic germinal centers (GCs) development and inflammation in t
198 n murine models of lupus is the formation of germinal centers (GCs) in lymphoid tissues where self-re
202 s that have passed this step generate normal germinal centers (GCs) upon a T-dependent immune challen
203 d with blood, although it is well known that germinal centers (GCs) within lymph nodes (LNs) serve as
204 at support B cell affinity maturation within germinal centers (GCs), resulting in the production of h
205 ls promote affinity maturation of B cells in germinal centers (GCs), whereas T follicular regulatory
211 ed the lymphoid follicle size (p < 0.01) and germinal centers (p < 0.01) with in the Peyer's patch we
212 ated with a significant reduction in induced germinal centers and CD4(+) germinal center T follicular
213 1 and SpiB in mature B cells do not generate germinal centers and high-affinity antibody after protei
215 T-bet from B cells impaired the formation of germinal centers and mitigated the development of kidney
216 in RasGRP1 and CD275 formed Tfh17 cells and germinal centers and produced similar titers of autoanti
217 xpression patterns typically associated with germinal centers and T follicular helper cells were exam
218 , and disruption of the formation of ectopic germinal centers are considered the main therapeutic tar
220 evelopment and affinity maturation occurs in germinal centers in lymphoid follicles through a critica
221 e the rapid appearance of autoantibodies and germinal centers in spontaneous murine models of systemi
222 tation and affinity maturation take place in germinal centers leading to the generation of memory B c
223 orly understood as selection taking place in germinal centers occurs on the basis of antibody affinit
225 suggest that FMDV persistence occurs in the germinal centers of lymphoid tissue but that the duratio
226 red humoral immunity as indicated by reduced germinal centers reactions, follicular CD4 T cells, and
227 cking IL-17R had fewer germinal centers, and germinal centers that formed contained fewer autoreactiv
228 develop mathematical models of Tfh cells in germinal centers to explicitly define the mechanisms of
229 of CD278 coordinate with their appearance in germinal centers, all attributes of T follicular helper
230 grp1-deficient mice lacking IL-17R had fewer germinal centers, and germinal centers that formed conta
231 new insights into the dynamic regulation of germinal centers, and suggesting more efficacious vaccin
232 minal center B cells, the size and number of germinal centers, and the frequency of SIV-specific Ab-s
233 ls; this caused the spontaneous formation of germinal centers, increased titers of serum autoantibodi
235 endritic cells, hindering B-cell division in germinal centers, which results in a delayed production
248 use a 3D GC organoid and show EZH2 mediates germinal centre (GC) formation through epigenetic silenc
249 igh-affinity antibody production through the germinal centre (GC) response is a pivotal process in ad
252 +) PC development pathway, namely (i) IgE(+) germinal centre (GC)-like B cells, (ii) IgE(+) PC-like '
253 l responses underlying the activation of the germinal centre activities leading to the generation of
254 on is sufficient to recruit B cells into the germinal centre and induce memory and plasma cell respon
255 lar dendritic cells, Tfh cells move into the germinal centre and provide help to B cells both by dire
257 cells, a reduction in B cell activation and germinal centre formation, and the inhibition of antigen
259 r helper (Tfh) cells is vital in driving the germinal centre reaction and high affinity antibody form
260 control the magnitude and specificity of the germinal centre reaction, but how regulation is containe
263 nization or infection, which localize to the germinal centre where they control the magnitude of the
265 cell help-undergo affinity maturation within germinal centres and persist as long-lived IgG plasma ce
266 ong-lived IgG plasma cells, which develop in germinal centres and then home to the bone marrow, IgM p
267 ents with synovial tissue containing ectopic germinal centres compared with diffuse synovial tissue.
272 ntly lower in the embryonic white matter and germinal matrix relative to the neocortex in both infant
275 lt rodent brain, new neurons are born in two germinal regions that are associated with blood vessels,
276 They can be derived from foetal or adult germinal tissues and continuously propagated in vitro as
277 ogenous betaine was present at low levels in germinal vesicle (GV) stage mouse oocytes before ovulati
278 ing proteolysis of cyclins and Cdc25B at the germinal vesicle (GV) stage, APC/C associated with the C
284 anic osmolyte, during vitrification of mouse germinal vesicle stage oocyte and/or subsequent maturati
286 ed by a TRP ion channel in immature oocytes (germinal vesicle stage), matured oocytes (metaphase II e
287 an oocyte involves a series of steps whereby germinal-vesicle oocytes (in which the nuclei are intact
289 e neurons derived from the zebrafish pallial germinal zone arrange in outside-in, age-related layers
290 velopment, Pax6 is robustly expressed in the germinal zone of all glutamatergic neurons [cerebellar n
291 The subventricular zone (SVZ) is the largest germinal zone of the forebrain and is responsible for th
292 lar plexus (SVP) extends through a hindbrain germinal zone populated by NPCs whose peak mitotic activ
295 ignificantly decreased cell proliferation in germinal zones and profound deficits in radial migration
297 s maintaining progenitor pools in cerebellar germinal zones, including cerebellar granule neuron prec
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