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1 ved that NKG2D deficiency affects peripheral B cell numbers.
2 eased marginal zone and decreased follicular B cell numbers.
3 nsgenic mice do not show increases in thymic B cell numbers.
4 effects on B cell survival and marginal zone B cell numbers.
5 n for BLyS/Bcmd signals regulates follicular B cell numbers.
6 ld leukocytosis, including elevated immature B cell numbers.
7 odeficiency in mice characterized by reduced B cell numbers.
8 anin and OVA, as well as reduced Ag-specific B cell numbers.
9 lvap deletion has no effect on IgM(+)IgD(lo) B cell numbers.
10 e mature B cells, albeit at >20-fold reduced B cell numbers.
11 tween peripheral blood eosinophil levels and B cell numbers.
12 e also associated with decreased circulating B cell numbers.
13 +) depletion triggered a potent expansion of B cell numbers.
14 ntibody levels and disease flare even at low B cell numbers.
15 bone marrow in an attempt to maintain normal B cell numbers.
16 nses are supported by close correlation with B cell numbers.
17 deletion of FADD led to increased peripheral B cell numbers.
18 py is associated with variable diminution in B cell numbers.
19 mmunoglobulin levels and in mature and total B cell numbers.
20 at is associated with a striking decrease in B-cell numbers.
21 luate a subset of patients with CVID and low B-cell numbers.
22 with significantly higher CSF CD4, CD8, and B-cell numbers.
23 with a concomitant increase in transitional B-cell numbers.
24 ularly of CD8(+) T cells, and reduced memory B-cell numbers.
25 kewing, with increased myeloid and decreased B-cell numbers.
26 f WASp+ T cells and limited correction in MZ B-cell numbers.
27 tment when most patients had recovered total B-cell numbers.
28 l increase in transitional and marginal zone B-cell numbers.
29 s and increased Tfh cell and germinal center B-cell numbers.
30 tive flow cytometry (HSFC), which can define B cell numbers 50-100 times lower than conventional tech
31 3 (KLF3, BKLF) increases marginal zone (MZ) B cell numbers, a phenotype shared with mice lacking KLF
32 c MLNs contain a 4.3-fold expansion in total B cell number and a 2.5-fold increased percentage of CD4
33 ese findings demonstrate that Klf4 regulates B cell number and activation-induced B cell proliferatio
35 The factor(s) responsible for the reduced B cell number and increased T cell infiltrate in T-cell-
37 gly reduced late transitional and follicular B cell numbers and are essentially devoid of marginal zo
38 Inc.) is suggested by its marked effects on B cell numbers and autoantibody formation as well as the
39 resulted in increased splenic and lymph node B cell numbers and decreased peritoneal B1 cell numbers.
43 nity as demonstrated by augmented CD4 TFH/GC B cell numbers and hastened islet allograft rejection in
46 e recurrent infections, despite normal T and B cell numbers and intact in vitro lymphocyte function.
47 on of serum autoantibody levels, normal host B cell numbers and MHC class II expression, reduced dono
49 ivo BLyS inhibition profoundly reduced naive B cell numbers and primary immune responses, it had a ma
51 Here, we observe an increase in follicular B cell numbers and selective recovery of the MZ B cell c
52 a longitudinal study to evaluate changes in B cell numbers and subpopulations that occur during the
56 ficant correlation between peripheral memory B-cell numbers and antibody levels for five of the eight
57 HSC-GT led to a progressive improvement in B-cell numbers and development, along with increased lev
60 differed from that seen in circulating naive B-cell numbers and in a cross-platform biomarker analysi
61 ration of BAFFR-Fc in mice reduced pulmonary B-cell numbers and prevented CS-induced formation of lym
62 nfants' blood samples were also analyzed for B-cell numbers and proportions of CD5(+) and CD27(+) B c
65 Less drastic reductions in marginal zone B cell numbers are also seen in the spleens of recombina
66 Although transitional immature type 1 (T1) B cell numbers are normal in Bim(-/-) mice, T2 and folli
69 his plasticity and despite constant renewal, B-cell numbers are stable in the absence of immunization
70 se model, we show that despite reduced total B cell numbers, B cell development in these mice occurs
71 e causes a progressive decline in peripheral B cell numbers, beginning at the transitional 1 developm
72 ted with B cell numbers, with flare at lower B cell numbers being associated with the highest BAFF le
73 in life, Rasgrp1-deficient mice have normal B cell numbers but are T lymphopenic, leading to defecti
74 D mice, btk deficiency only modestly reduces B cell numbers, but dramatically protects against diabet
77 reatment in 5-wk-old NOD female mice reduced B cell numbers by approximately 95%, decreased subsequen
79 the patients in whom the marked decrease in B cell numbers characteristic of XLA could not be confir
80 t L chain receptor editing responses and had B cell numbers comparable to those found in animals lack
82 icant decrease in absolute live or total CLL B-cell numbers, confirming that trogocytosis occurs, rat
84 of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expre
86 or repeated vaccinations were common, memory B-cell numbers did not correlate with antibody titers.
88 n Glut1 and Mcl-1 levels, glucose uptake and B cell number in the absence of TRAF3 were all dependent
89 ernative NF-kappaB activation and peripheral B cell numbers in a BAFF-R-dependent manner, whereas unc
90 ormal in TTT/AAA beta2-integrin KI mice, but B cell numbers in lymph nodes and IgG and IgM production
91 ciated with drastic reductions in peripheral B cell numbers in Mdm2(+/-)E micro -myc transgenics, and
93 cy enhanced CD4 TFH and germinal center (GC) B cell numbers in naive mice and hastened islet allograf
94 analyzed various molecular markers of T and B cell numbers in neonatal dried blood spots of 99 child
95 hese changes produced a drastic reduction in B cell numbers in spleen and blood, and a novel increase
98 ited to a single normal D(H) achieved normal B cell numbers in the periphery, mice forced to preferen
100 trabecular bone (-61%), and markedly reduced B-cell number in the marrow (-52%) and blood (-36%) comp
102 Similar to CD4(+) but not CD8(+) T cells, B-cell numbers in both groups increased significantly af
104 atients had stable/improved cGVHD, and total B-cell numbers in these patients were significantly high
106 In response to a high-cholesterol diet, IRA B cell numbers increase preferentially in secondary lymp
109 eover, they suggest that estrogen control of B cell number is indirect via osteocytes and that the in
112 igation activity and severely reduced mature B cell numbers, Lig4(R278H/R278H) (Lig4(R/R)) mice exhib
113 especially robust increases in transitional B cell number, marginal zone B cell proliferation, and C
114 with loss of serum Igs: 1) increased splenic B-cell numbers, mostly of the B1 and marginal zone (MZ)
115 t recirculation accounts for the decrease in B cell numbers observed in secondary lymphoid organs.
116 en receptor alpha from B cells did not alter B cell number or bone mass and did not alter the respons
117 ions of autoreactive B cells, we found total B cell numbers paradoxically reduced in HCV-infected pat
123 l center formation and reduced marginal zone B cell numbers, similar to a pan-class I inhibitor.
124 ow, concomitant with the increase in splenic B cell number, suggest that redistribution of circulatin
125 n had a approximately 50% loss in follicular B cell numbers, suggesting that escape from central tole
127 of antiviral Ab responses, including splenic B cell numbers, survival and function of adoptively tran
129 models lacking RANK or RANKL show defects in B cell number, the role of the RANKL-RANK axis on B phys
131 troduction of Rel protein restored wild-type B cell numbers to mice reconstituted with PU.1(+/-)Spi-B
138 splantation, with no IS, CD4 T-cell and CD20 B-cell numbers were increased, but were reduced by IS.In
143 ers were normal, but naive mature and memory B-cell numbers were reduced despite slightly increased s
144 ffect of 5 days of IL-4 treatment on splenic B cell number when B lymphopoiesis is blocked with anti-
145 urvival was studied by evaluating changes in B cell number when lymphopoiesis was suppressed with ant
146 p300 led to surprisingly modest deficits in B-cell numbers, whereas inactivation of both genes was n
147 o a pronounced global reduction in mature B2 B cell numbers, which correlated with impaired survival
148 By contrast, DeltaBAFF/3H9 mice had reduced B cell numbers with a repertoire similar to that of 3H9
149 acteristic shift in dark zone and light zone B cell numbers, with an increase of B cells in the dark
150 m BAFF levels were inversely correlated with B cell numbers, with flare at lower B cell numbers being
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