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1 of priming immunogens that induce rare bnAb-precursor B cells.
2 this process in mice carrying V3-glycan bNAb precursor B cells.
3 istration rescue anergic Env(+) (non-edited) precursor B cells.
4 the expression of naked IgL on a surface of precursor B cells.
5 e bnAb induction by activating bnAb germline precursor B cells.
6 e, replenishment must involve replication of precursor B cells.
7 ication artifacts and are unique to leukemic precursor B cells.
8 D86, but not CD80, on follicular, MZ, and MZ precursor B cells.
9 ice despite a significant loss of H3K9me2 in precursor B cells.
10 d recombination of Iglambda gene segments in precursor B cells.
11 n from B220+CD43+ progenitor B to B220+CD43- precursor B cells.
12 Ab induction is vaccine priming of rare bnAb-precursor B cells.
13 dine deaminase (AID; also known as AICDA) in precursor B-cells.
14 y and correlate with poor prognosis in human precursor B cell acute lymphoblastic leukemia (B-ALL).
15 Ikaros (IKZF1) is a hallmark of BCR-ABL1(+) precursor B cell acute lymphoblastic leukemia (pre-B ALL
18 IKAROS function indicates poor prognosis in precursor B-cell acute lymphoblastic leukemia (B-ALL).
19 To test the suitability of targeting CD22 on precursor B-cell acute lymphoblastic leukemia (BCP-ALL),
21 d on xenografts from pediatric patients with precursor B-cell acute lymphoblastic leukemia (pre-B ALL
24 amics during CD19 CAR T-cell therapy against precursor B-cell acute lymphocytic leukemia (B-ALL).
26 the clonal evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is ch
27 ecently been established from a patient with precursor-B-cell acute lymphoblastic leukemia (ALL), whi
28 and TCF3-PBX1 (E2A-PBX1)-frequently found in precursor-B-cell acute lymphoblastic leukemia (preB-ALL)
30 w cytometric assay to identify patients with precursor B-cell ALL (B-ALL) at very low risk (VLR) of r
32 rmed genomic profiling of 1725 patients with precursor B-cell ALL and detailed genomic analysis of 15
34 r patients with PGR in the large subgroup of precursor B-cell ALL, dexamethasone especially reduced t
36 ined that LOH of 6q was demonstrated both in precursor-B cell ALLs (15 of 93; 16%) and in T cell ALLs
39 caused no change in the cell cycle status of precursor B cells and only modest changes in cycling pro
40 up-regulation of CD86(high) expression on MZ precursor B cells and trafficking of MZ precursor B cell
42 lete loss of marginal zone and marginal zone precursor B cells, and 'preferential' population expansi
43 on of plasmacytoid dendritic cells (DCs), MZ precursor B cells, and CD4 T cells in the spleens of BXD
44 ular mimicry in Graves' disease, where early precursor B cells are expanded by Y. enterocolitica pori
45 ified impaired Ig locus contraction in adult precursor B cells as a likely mechanism by which ID2-med
46 ferentiation into germinal center and memory precursor B cells as well as preplasmablasts that rapidl
48 competition of broadly neutralizing antibody precursor B cells at a physiological precursor frequency
49 ings expand the range of NF-kappaB action in precursor B cells beyond Igkappa to include the control
50 ntified on splenic marginal zone (MZ) and MZ precursor B cells, but not on the bulk of newly formed B
51 arily to B lymphocytes and can be induced in precursor B cells by stimulation with bacterial lipopoly
52 n IFN receptor-intact BXD2 mouse spleens, MZ precursor B cells clustered at the T cell-B cell border.
54 49F) and IL-7Ralpha(-/-) mice had comparable precursor B cell defects, indicating that signaling from
57 ed in a blockage of the progenitor B-cell-to-precursor B-cell development in bone marrow (BM) and B-c
60 dependent on sufficient levels of IL-7 than precursor B cell differentiation because the number of B
61 pproximating human conditions of VRC01-class precursor B cell diversity, affinity, and frequency, tha
63 The transcription factor E2A can promote precursor B cell expansion, promote G(1) cell cycle prog
64 se renin-expressing progenitors enriches the precursor B-cell gene programme and constrains lymphocyt
67 rturbs B-cell development, as evidenced by B-precursor/B-cell hyperplasia, and corrupts the regulatio
68 unogens that primed responses from rare bnAb-precursor B cells in a mouse model and bound a range of
69 of the HCDR3-dominant bnAb BG18, primed bnAb-precursor B cells in eight of eight rhesus macaques to s
70 he nucleus of progenitor B (pro-B) and large precursor B cells in the bone marrow, an expression patt
71 69 and CD86 observed in RBP(+) marginal zone precursor B cells in the spleens of BXD2 mice compared w
74 pment, is required for entry of activated GC precursor B cells into the germinal center reaction; del
75 -ALL, overexpression of TET1 alone in normal precursor B cells is sufficient to transform the cells a
76 LBL (T-LBL) and six (8%) of 73 patients with precursor B-cell LBL (pB-LBL) suffered from relapse.
77 uption of the NF-kappaB signaling pathway in precursor B cells led to the loss of inducible Oct-2 DNA
78 Children younger than 6 years of age with precursor B-cell leukemia and no adverse genetic feature
79 with chemotherapy, whereas patients who have precursor B-cell leukemia without other adverse features
82 BG18-like HIV broadly neutralizing antibody-precursor B cells (<1-in-50 million) in non-human primat
83 nt patient with Epstein-Barr virus-negative, precursor B cell lymphoblastic lymphoma diagnosed 6 mont
86 HistoryAn 18-year-old man was diagnosed with precursor B-cell lymphoblastic leukemia and underwent tr
87 istory An 18-year-old man was diagnosed with precursor B-cell lymphoblastic leukemia and underwent tr
89 This translocation is mainly acquired in precursor B cells mediated by recombination-activating g
91 ned two HIV-1 envelope immunogens that bound precursor B cells of either a CD4 binding site or V3-gly
92 er(fl/fl)/Emicro-myc mice were of very early precursor B-cell origin, a stage of B-cell development p
94 serve to distinguish between the presumed MZ precursor B cell population in the spleen and other IgD-
95 ontrol the progenitor B cell (pro-B cell) to precursor B cell (pre-B cell) transition have not been w
96 ates with GC sensitivity in a panel of human precursor B-cell (pre-B) acute lymphoblastic leukemia (A
97 ment of progenitor B cells (ProB cells) into precursor B cells (PreB cells) is dictated by immunoglob
101 e critical for maintaining quiescence before precursor B cell receptor (pre-BCR) expression and for r
102 difficult by low frequencies of appropriate precursor B cell receptors and the complex maturation pa
104 truncated/V(H)-less mouse H chain Dmu forms precursor B cell receptors with the surrogate L chain co
105 expression of Blimp-1 in Abelson-transformed precursor B cells repressed endogenous c-Myc and caused
107 ild-type and IL-33-deficient pro-B and large precursor B cells revealed a unique, IL-33-dependent tra
108 rate stages: First, activate the appropriate precursor B cells; second, shepherd affinity maturation
109 ms behind are still unknown, we studied five precursor B cell subsets (ProB, PreBI, PreBII large, Pre
111 bs are important vaccine leads because their precursor B cells targeted by an engineered priming immu
112 approximately 10 times fewer virus-specific precursor B cells than normal spleen cells, had no signi
113 sis revealed intragraft differentiation from precursor B cells to memory B cells in accepted allograf
114 and recruited broadly neutralizing antibody precursor B cells to the GC response more efficiently co
115 n MZ precursor B cells and trafficking of MZ precursor B cells to the T cell-B cell border to provide
116 gH) locus and a block in the progenitor-B-to-precursor-B-cell transition, which was partially rescued
117 ion or pneumovirus cross-neutralization from precursor B cells with low initial affinity for the RSV-
118 scaffold nanoparticles can elicit rare bnAb-precursor B cells with predefined binding specificities