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1 ction in peripheral T cells without reducing B cell number.
2 n cGVHD mice were not merely a reflection of B-cell number.
3 ure B cells, resulting in reduced peripheral B cell numbers.
4 small lymph nodes with marked reductions in B cell numbers.
5 py is associated with variable diminution in B cell numbers.
6 mmunoglobulin levels and in mature and total B cell numbers.
7 d, to a greater extent, germinal center (GC) B cell numbers.
8 nsgenic mice do not show increases in thymic B cell numbers.
9 effects on B cell survival and marginal zone B cell numbers.
10 ved that NKG2D deficiency affects peripheral B cell numbers.
11 n for BLyS/Bcmd signals regulates follicular B cell numbers.
12 ld leukocytosis, including elevated immature B cell numbers.
13 eased marginal zone and decreased follicular B cell numbers.
14 odeficiency in mice characterized by reduced B cell numbers.
15 anin and OVA, as well as reduced Ag-specific B cell numbers.
16 he numbers of peripheral T cells, but normal B cell numbers.
17 is suboptimal immune recovery with low T and B cell numbers.
18 pulp area with a significant decline in the B cell numbers.
19 s together with an increase in marginal zone B cell numbers.
20 lvap deletion has no effect on IgM(+)IgD(lo) B cell numbers.
21 e mature B cells, albeit at >20-fold reduced B cell numbers.
22 tween peripheral blood eosinophil levels and B cell numbers.
23 mpared to controls despite normal peripheral B cell numbers.
24 e also associated with decreased circulating B cell numbers.
25 +) depletion triggered a potent expansion of B cell numbers.
26 ntibody levels and disease flare even at low B cell numbers.
27 bone marrow in an attempt to maintain normal B cell numbers.
28 nses are supported by close correlation with B cell numbers.
29 deletion of FADD led to increased peripheral B cell numbers.
30 s and increased Tfh cell and germinal center B-cell numbers.
31 at is associated with a striking decrease in B-cell numbers.
32 luate a subset of patients with CVID and low B-cell numbers.
33 with significantly higher CSF CD4, CD8, and B-cell numbers.
34 with a concomitant increase in transitional B-cell numbers.
35 ularly of CD8(+) T cells, and reduced memory B-cell numbers.
36 ing memory Treg cells, but not higher IgE(+) B-cell numbers.
37 kewing, with increased myeloid and decreased B-cell numbers.
38 f WASp+ T cells and limited correction in MZ B-cell numbers.
39 tment when most patients had recovered total B-cell numbers.
40 l increase in transitional and marginal zone B-cell numbers.
41 had higher total B and CD27(+) IgA(+) memory B-cell numbers (15.2% [95% CI 3.2; 28.7], 22.5% [95% CI
42 tive flow cytometry (HSFC), which can define B cell numbers 50-100 times lower than conventional tech
43 3 (KLF3, BKLF) increases marginal zone (MZ) B cell numbers, a phenotype shared with mice lacking KLF
44 c MLNs contain a 4.3-fold expansion in total B cell number and a 2.5-fold increased percentage of CD4
45 ese findings demonstrate that Klf4 regulates B cell number and activation-induced B cell proliferatio
47 The factor(s) responsible for the reduced B cell number and increased T cell infiltrate in T-cell-
49 greater airway dysfunction, while increased B cell numbers and altered monocyte subsets were associa
50 gly reduced late transitional and follicular B cell numbers and are essentially devoid of marginal zo
51 Inc.) is suggested by its marked effects on B cell numbers and autoantibody formation as well as the
52 resulted in increased splenic and lymph node B cell numbers and decreased peritoneal B1 cell numbers.
56 nity as demonstrated by augmented CD4 TFH/GC B cell numbers and hastened islet allograft rejection in
59 in hematopoietic stem cells severely reduced B cell numbers and impaired B cell development in a hema
60 e recurrent infections, despite normal T and B cell numbers and intact in vitro lymphocyte function.
61 on of serum autoantibody levels, normal host B cell numbers and MHC class II expression, reduced dono
63 ivo BLyS inhibition profoundly reduced naive B cell numbers and primary immune responses, it had a ma
65 Here, we observe an increase in follicular B cell numbers and selective recovery of the MZ B cell c
66 a longitudinal study to evaluate changes in B cell numbers and subpopulations that occur during the
70 ficant correlation between peripheral memory B-cell numbers and antibody levels for five of the eight
71 HSC-GT led to a progressive improvement in B-cell numbers and development, along with increased lev
74 differed from that seen in circulating naive B-cell numbers and in a cross-platform biomarker analysi
75 ration of BAFFR-Fc in mice reduced pulmonary B-cell numbers and prevented CS-induced formation of lym
76 nfants' blood samples were also analyzed for B-cell numbers and proportions of CD5(+) and CD27(+) B c
78 es, decreased T cell infiltration, increased B cell numbers, and decreased macrophage recruitment.
80 Less drastic reductions in marginal zone B cell numbers are also seen in the spleens of recombina
82 Although transitional immature type 1 (T1) B cell numbers are normal in Bim(-/-) mice, T2 and folli
85 his plasticity and despite constant renewal, B-cell numbers are stable in the absence of immunization
87 se model, we show that despite reduced total B cell numbers, B cell development in these mice occurs
88 e causes a progressive decline in peripheral B cell numbers, beginning at the transitional 1 developm
89 ted with B cell numbers, with flare at lower B cell numbers being associated with the highest BAFF le
90 in life, Rasgrp1-deficient mice have normal B cell numbers but are T lymphopenic, leading to defecti
91 D mice, btk deficiency only modestly reduces B cell numbers, but dramatically protects against diabet
94 reatment in 5-wk-old NOD female mice reduced B cell numbers by approximately 95%, decreased subsequen
96 the patients in whom the marked decrease in B cell numbers characteristic of XLA could not be confir
97 t L chain receptor editing responses and had B cell numbers comparable to those found in animals lack
98 Treg, Treg-memory, and CD27(+) IgA(+) memory B-cell numbers compared to children without atopic disea
100 icant decrease in absolute live or total CLL B-cell numbers, confirming that trogocytosis occurs, rat
102 of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expre
104 or repeated vaccinations were common, memory B-cell numbers did not correlate with antibody titers.
106 etion increases bacterial burden and reduces B cell numbers, IgG release, and neutrophil stimulation.
107 llowed for at least 24 months had sufficient B-cell numbers, IgM concentration, or IgM isohemagglutin
108 n Glut1 and Mcl-1 levels, glucose uptake and B cell number in the absence of TRAF3 were all dependent
109 ernative NF-kappaB activation and peripheral B cell numbers in a BAFF-R-dependent manner, whereas unc
110 d that conditions associated with reduced MZ B cell numbers in adult mice cause increased cDC2 occupa
111 ormal in TTT/AAA beta2-integrin KI mice, but B cell numbers in lymph nodes and IgG and IgM production
112 ciated with drastic reductions in peripheral B cell numbers in Mdm2(+/-)E micro -myc transgenics, and
114 cy enhanced CD4 TFH and germinal center (GC) B cell numbers in naive mice and hastened islet allograf
115 analyzed various molecular markers of T and B cell numbers in neonatal dried blood spots of 99 child
116 hese changes produced a drastic reduction in B cell numbers in spleen and blood, and a novel increase
119 ited to a single normal D(H) achieved normal B cell numbers in the periphery, mice forced to preferen
121 trabecular bone (-61%), and markedly reduced B-cell number in the marrow (-52%) and blood (-36%) comp
123 Similar to CD4(+) but not CD8(+) T cells, B-cell numbers in both groups increased significantly af
124 sociations of higher Treg and CD27(+) IgA(+) B-cell numbers in children with food-allergic sensitizat
125 ch did not show decreases in CD4+, CD8+, and B-cell numbers in the pancreas and draining lymph nodes,
127 atients had stable/improved cGVHD, and total B-cell numbers in these patients were significantly high
129 In response to a high-cholesterol diet, IRA B cell numbers increase preferentially in secondary lymp
132 eover, they suggest that estrogen control of B cell number is indirect via osteocytes and that the in
135 igation activity and severely reduced mature B cell numbers, Lig4(R278H/R278H) (Lig4(R/R)) mice exhib
136 especially robust increases in transitional B cell number, marginal zone B cell proliferation, and C
137 with loss of serum Igs: 1) increased splenic B-cell numbers, mostly of the B1 and marginal zone (MZ)
138 t recirculation accounts for the decrease in B cell numbers observed in secondary lymphoid organs.
140 en receptor alpha from B cells did not alter B cell number or bone mass and did not alter the respons
141 ions of autoreactive B cells, we found total B cell numbers paradoxically reduced in HCV-infected pat
144 e patients with the highest gene marking and B-cell numbers remain off immunoglobulin replacement the
148 l center formation and reduced marginal zone B cell numbers, similar to a pan-class I inhibitor.
150 ow, concomitant with the increase in splenic B cell number, suggest that redistribution of circulatin
151 n had a approximately 50% loss in follicular B cell numbers, suggesting that escape from central tole
153 of antiviral Ab responses, including splenic B cell numbers, survival and function of adoptively tran
155 models lacking RANK or RANKL show defects in B cell number, the role of the RANKL-RANK axis on B phys
157 of ER protein folding capacity and increased B-cell number through survival pathways and cell replica
158 tor 11 (GDF11), nodal], and the expansion of B-cell number through various mechanisms including trans
159 troduction of Rel protein restored wild-type B cell numbers to mice reconstituted with PU.1(+/-)Spi-B
169 IgM(+) (70-80%), but IgA(+) (and not IgG(+)) B-cell numbers were increased in LFs from severe COPD co
170 splantation, with no IS, CD4 T-cell and CD20 B-cell numbers were increased, but were reduced by IS.In
175 ers were normal, but naive mature and memory B-cell numbers were reduced despite slightly increased s
176 ffect of 5 days of IL-4 treatment on splenic B cell number when B lymphopoiesis is blocked with anti-
177 urvival was studied by evaluating changes in B cell number when lymphopoiesis was suppressed with ant
178 p300 led to surprisingly modest deficits in B-cell numbers, whereas inactivation of both genes was n
179 o a pronounced global reduction in mature B2 B cell numbers, which correlated with impaired survival
180 and influenza heamaglutinin-specific memory B-cell numbers, which phenotypically differs from vaccin
181 By contrast, DeltaBAFF/3H9 mice had reduced B cell numbers with a repertoire similar to that of 3H9
182 acteristic shift in dark zone and light zone B cell numbers, with an increase of B cells in the dark
183 m BAFF levels were inversely correlated with B cell numbers, with flare at lower B cell numbers being