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1 g animals, despite significant reductions in T cell number.
2 tive cell death prevents further increase in T cell number.
3 -2-mediated control of memory phenotype CD8+ T cell number.
4 and it was accompanied by reduced regulatory T cell number.
5 ice showed a 2- to 3-fold increase in memory T cell number.
6 asis by counteracting transient increases in T-cell number.
7 s were negatively correlated with regulatory T cell numbers.
8 rely diminished mucosal-associated invariant T cell numbers.
9 node) displayed no such increases in CD8(+) T cell numbers.
10 immune responsiveness or T reg and effector T cell numbers.
11 ymic output, potentially reducing peripheral T cell numbers.
12 tween naive, memory, and Foxp3(+) regulatory T cell numbers.
13 tantly decreased inflammatory and regulatory T cell numbers.
14 ed in Tbx21(-/-) mice by reducing regulatory T cell numbers.
15 fication of cytokine profiles and regulatory T cell numbers.
16 ere cytokine secretion levels and regulatory T cell numbers.
17 otype and a selective decrease in regulatory T cell numbers.
18 (DN1) stage, leading to decreased peripheral T cell numbers.
19 ollowed by an equally extensive reduction in T cell numbers.
20 tion was accompanied by a decrease in NK and T cell numbers.
21 substantial than the reduction of total CD4 T cell numbers.
22 This resulted in a 1400-fold increase in T cell numbers.
23 moter display a 10-20-fold increase in total T cell numbers.
24 during persistence, in contrast to declining T cell numbers.
25 iated contraction and do not increase memory T cell numbers.
26 e can enhance NK cell and tumor-specific CD8 T cell numbers.
27 ions between LLP2A signal and macrophage and T cell numbers.
28 in mice results in diminished peripheral CD8 T cell numbers.
29 ports, did not lead to an increase in memory T cell numbers.
30 it did not alter conventional CD4(+)Foxp3(-) T cell numbers.
31 gen-presenting capacity of DCs and increased T-cell numbers.
32 al enumeration of total and antigen-specific T-cell numbers.
33 r peripheral deletion to maintain peripheral T-cell numbers.
34 rease in circulating CD4(+) T-cell and naive T-cell numbers.
35 the HIV-1-controllers with diminished CD4(+)T-cell numbers.
36 e with BCG in inducing Ag85B-specific CD4(+) T-cell numbers.
37 with a marked decrease in splenic gammadelta T-cell numbers.
38 elimination of the latter decreasing CD4(+) T-cell numbers.
39 D, with no significant differences in CLA(-) T-cell numbers.
40 natural killer, T helper 17, and regulatory T-cell numbers.
41 infections, despite normal peripheral CD4(+) T-cell numbers.
42 lated with ~500% increase in effector CD8(+) T-cell numbers.
43 eased circulating CD25(+) T cells and CD4(+) T-cell numbers.
44 oire formation, receptor editing, and B- and T-cell numbers.
45 ry encompassed the recovery of normal CD4(+) T cell numbers, a low ratio of effector to central memor
46 31 induces profound reduction of peripheral T cell numbers after oral dosage and confers pronounced
47 4+ T-cell numbers were lower than naive CD8+ T-cell numbers; after HAART, a greater increase in naive
48 in a marked relative increase in regulatory T-cell numbers among the CD4 T-cell subset of the challe
49 ally in T cells led to a strong reduction in T cell number and a shift toward the effector/memory phe
51 ne the effect of gammaherpesvirus latency on T cell number and differentiation during subsequent hete
53 e can be modulated by preexisting memory CD8 T cell number and the intensity of inflammation during r
55 70% reduction in activated CD4(+) and CD8(+) T cell numbers and 20-50% reductions in IFN-gamma-produc
56 Absence of CD18 led to diminished CD4+CD25+ T cell numbers and affected both thymic and peripheral d
57 After one or two inoculations of MVA, the T cell numbers and antibody titers equaled or exceeded t
59 y to LNG-treated mice at 1 dpi restored lung T cell numbers and chlamydial burden at 12 dpi to levels
60 T cells resulted in decreased peak donor CD8 T cell numbers and decreased CTL effector function due t
61 matically increased Vbeta14(+) thymocyte and T cell numbers and decreased numbers of cells expressing
62 revealed a positive association between CD8 T cell numbers and decreased proinflammatory function of
63 iency in T cells led to decreased peripheral T cell numbers and defective homeostatic proliferation,
64 slow and causes a gradual increase in total T cell numbers and differentiation into cells with featu
65 -/-) mice display a slight reduction in CD8+ T cell numbers and do not effectively clear a pulmonary
66 er, viral peptide-specific CD4(+) and CD8(+) T cell numbers and effector cell development were signif
67 nt viral infection erodes virus-specific CD8 T cell numbers and effector function, with a concomitant
68 ession on hematopoietic cells inhibited CD8+ T cell numbers and function after LCMV CL-13 infection.
70 rol the risk of leukemia, we assessed NK and T cell numbers and function in IL-2Rgamma(c)(-/-) mice r
72 rance, but increased IL-22 in vivo decreased T cell numbers and functions in the liver and lymphoid t
73 o partially restore NY-ESO-1-specific CD8(+) T cell numbers and functions, increasing the likelihood
75 milarly, a significant decrease was noted in T cell numbers and in CD45RB(low) (activated/memory) exp
77 only 3% of wild-type CD45 activity restored T cell numbers and normal cytotoxic T cell responses.
78 amma (IFN-gamma) expression, increases naive T cell numbers and reduces effector T cell numbers in ad
79 ion with IL-15 boosted antigen-specific CD8+ T cell numbers and resulted in a cooperative effect on t
80 spleens were studied at intervals for B and T cell numbers and subsets and frequency of anti-double-
85 14-day Ang II infusion increased gammadelta T-cell numbers and activation in the spleen of wild-type
86 with poor prognosis, in addition to reduced T-cell numbers and activity with disease transformation.
89 ry T-cell regeneration that preserves CD4(+) T-cell numbers and functions above the threshold associa
90 Cs during T-cell priming, whereas allogeneic T-cell numbers and homing in lymphoid and GVHD target or
91 ific HLA multimers to enumerate CMV-specific T-cell numbers and select cells to assess chimerism stat
92 found that Neu5Gc exposure reduced IL-17(+) T-cell numbers and supported differentiation of regulato
93 regression after SCT, absolute WT1(+) CD8(+) T-cell numbers and WT1 expression were studied for each
94 r vaccination, absolute PR1 and WT1(+)CD8(+) T-cell numbers and WT1 expression were studied weekly af
95 in TIL cultures was associated with reduced T cell numbers, and further functional studies demonstra
96 uced lung eosinophilia, changes in pulmonary T cell numbers, and gene and protein expression as well
98 nd bacterial burden, restored splenic CD4(+) T-cell numbers, and increased the frequency of Ehrlichia
99 CD4(+) T-cell frequencies, decreased CD8(+) T-cell numbers, and resolution of CD8(+) T-cell alveolit
100 nd angiogenic capacities of EPCs, angiogenic T-cell numbers, and vascular endothelial growth factor e
103 how in this article that circulating Vdelta1 T cell numbers are particularly high in patients with HI
104 Competition for these ligands declines when T cell numbers are reduced and causes residual naive T c
106 ses in inflammation, coagulation, and CD8(+) T-cell numbers are associated with an elevated cardiovas
107 ric PTLD patients, pretreatment EBV-specific T-cell numbers are in the range of healthy controls.
109 ete lack of B cells and dramatically reduced T cell numbers, as shown by Rag1(-/-) blastocyst complem
111 ation and apparent proliferation, with large T cell numbers at the Ag-positive tumor as early as day
113 patients had profound defects in CD4 and CD8 T-cell numbers at diagnosis that did not recover during
114 served a transient increase in CD4+ and CD8+ T-cell numbers at the residual tumor after androgen abla
115 adually exceeded bystander p18-specific CD8+ T-cell numbers, both populations peaked concurrently wit
116 proliferation is suppressed by increases in T cell numbers but not by adoptive transfer of regulator
117 significantly increased Ag-specific effector T cell numbers, but does not result in increased numbers
118 nced IL-2 signals increase peak effector CD8 T cell numbers, but only early IL-2 signals enhance memo
119 e manipulated to improve HIV-specific CD8(+) T cell numbers, but possibly not all functions in vivo.
120 pathogen reencounter increases memory CD8(+) T cell numbers, but the impact on memory CD8(+) T cell d
121 gh negative regulation of natural regulatory T cell numbers by inhibiting the development of MHCII(lo
122 ific regulatory T cells, boosting regulatory T cell numbers by injecting IL-2 immune complexes dampen
124 rs, and strategies to amplify tumor-reactive T-cell numbers by immunization or ex vivo expansion foll
125 Many studies have shown that amplifying T-cell numbers by prime-boost vaccination is most effect
126 ation only had a modest impact on recovering T cell numbers, CD8+ T cells from vaccinated patients co
127 CTLA-4 blockade resulted in lower memory CD8 T cell numbers compared with the DC+early IL-2 treatment
131 Upon challenge with Y. pestis, pulmonary T-cell numbers decline in naive mice, whereas immunized
133 urthermore, after SHIV-89.6P infection, CD4+ T-cell numbers declined less and survival was longer in
138 ress to simian AIDS and that maintain stable T-cell numbers despite high levels of viral replication
140 spontaneous EAE, the number of MBP-specific T cell numbers does not build up gradually in the CNS; i
142 Lckcre(tg) Grb2-deficient mice show reduced T cell numbers due to impaired negative and positive sel
146 onse to antigen stimulation to confer CD8(+) T cell-number expansion and effector functions against d
147 cell survival and fitness during peripheral T cell-number expansion in response to virus infection.
148 between virus and host that occurs when CD4+ T cell numbers fall below a level that can sustain immun
149 on, E2F1/E2F2 DKO mice do not recover normal T cell numbers following exposure to a sublethal dose of
150 f therapeutic avenues aimed at modulating DN T cell number for the prevention of autoimmune diseases.
151 ent reduction in mean circulating CD25+ CD4+ T cell number, from 83 +/- 16 cells/microl to a nadir of
154 f the transferred T cells, even after stable T cell numbers have been reached, suggests that active c
155 in either CD30 or OX40 alone reduced CD4(+) T cell numbers, however, in mice deficient in both OX40
156 upon reactivation and preexisting memory CD8 T cell number (i.e., primary memory CD8 T cell precursor
157 ulation blockade also reduced virus-specific T-cell numbers, illustrating that sustained interactions
158 icant increases in dendritic cell and CD8(+) T cell number in advanced tumor-bearing mice compared wi
161 in psoriasis pathogenesis, but inflammatory T cell numbers in blood, as well as the relative importa
162 gnificantly increased median B cell, but not T cell numbers in both cohorts, with a trend for increas
163 led to a marked reduction of eosinophil and T cell numbers in bronchoalveolar lavage fluid compared
167 to reduced virus titers and increased CD8(+) T cell numbers in high- but not low-pathological infecti
169 K cells and contraction of CD4(+) and CD8(+) T cell numbers in individual patients in vivo provides s
170 es were profoundly reduced in blood, whereas T cell numbers in lymph nodes and spleen were at or near
173 y lymphoid organs, whereas it expanded naive T cell numbers in nonlymphoid tissues; these effects wer
176 l therapy (cART) substantially restores CD4+ T cell numbers in peripheral blood, but the gut compartm
180 We observed increases in OVA-specific CD8(+) T cell numbers in the local lung compartments (bronchoal
186 STC1 had minimal effects, however, on both T-cell number in the glomeruli and interstitium and on c
188 limus resulted in a decrease in host splenic T-cell numbers in anti-CD40L mAb-treated recipients.
190 t(W-sh/W-sh) hosts correlated with increased T-cell numbers in lymph nodes, liver, and gastrointestin
191 lted in enhanced thymopoiesis and peripheral T-cell numbers in middle-aged recipients of an allogenei
193 reduction in dendritic epidermal gammadelta T-cell numbers in the epidermis, indicating that these p
194 esults in dramatically decreased CD4 and CD8 T-cell numbers in the lamina propria of both small and l
195 were followed by relatively high and stable T-cell numbers in the SIV-infected macaques with a slow-
196 lecule, they have the potential to influence T-cell numbers in the skin through chemokine production
197 been linked to a failure to normalize CD4(+) T-cell numbers in treated human immunodeficiency virus (
200 uced spleen and lymph node CD4(+) and CD8(+) T cell numbers, including naive, activated, and Foxp3(+)
201 ction with vaccinia virus, dermal gammadelta T cell numbers increased 10-fold in the infected ear and
205 ited T cell reconstitution, decreased memory T cell numbers, increased the relative frequency of Treg
206 0-enhancement of tumor immunity and effector T cell numbers is decreased in middle-aged mice and was
207 ermine whether the quantitative reduction in T-cell numbers is due to an intrinsic T-cell defect or w
208 a is that the age-related rate of decline of T-cell numbers is slower in patients than controls.
209 Although the age-related fall in CD8(+) T-cell numbers is well established, neither the underlyi
211 rapy dramatically increased antigen-specific T-cell numbers leading to enhancement in the survival of
212 n-induced cell death, IL-21 sustained CD8(+) T cell numbers long term as a result of increased surviv
213 individuals is often characterized by lower T cell numbers, lower naive/memory T cell ratios, and lo
215 tion and that a physiological increase in DN T cell number may be sufficient to confer resistance to
216 pression (IFN-gamma, STAT-1, granzyme B) and T cell numbers may be due to a reduction in DC-mediated
219 the precursor B-cell development, low B- and T-cell numbers, normal immunoglobulin gene use, limited
221 erations in cytokine expression, the reduced T-cell numbers observed coincided with diminished T-cell
223 ase states that result in deficits in CD4(+) T cell numbers or function, such as may be seen in human
225 on from diabetes did not result from altered T cell numbers or subset distributions, or regulatory/su
226 elated T-cell expansions do not impair naive T-cell numbers or maintenance of protective responses ag
227 o infection, and did not increase memory CD8 T cell numbers over those observed in wild-type controls
230 ma, demonstrating an increase in circulating T cell numbers, particularly naive (TREC+) T cells.
231 t lesion macrophage-positive area and CD4(+) T-cell number per lesion area, but reduced lesion expres
238 plantation in rATG-treated patients, whereas T-cell numbers remained stable in both control groups.
239 ilamentous bacteria (SFB) partially restored T cell numbers, suggesting that SFB and other MMb organi
242 taining elevated insulin-specific regulatory T cell numbers that efficiently lowered diabetogenic eff
244 apy stimulated significant increases in CD8+ T cell numbers, the number of CD4+ T cells remained unch
245 roliferation does not normally fully restore T-cell numbers, the CD8(+) T-cell pool was completely re
247 , leading to reductions in pathologic DC and T-cell numbers to nonlesional levels; and (3) inhibition
249 thogen exposure, increased pathogen-specific T cell numbers together with altered migratory patterns
251 had a 60-fold increase in CD4(+)IFN-gamma(+) T cell numbers versus control animals at 2 wk post-needl
252 r gene-reporter probe systems for imaging of T cell number was performed, and the hNET/(18)F-MFBG PET
254 iter for all antigens, and decreasing CD4(+) T cell numbers was strongly associated with a decrease i
256 T cells, and the increase in tumor-specific T-cell number was due to reduced activation-induced cell
258 in the percentage of CD4+ and CD8+ cells and T-cell numbers was observed in 48%, 71% and 99% of LTRs.
259 ddition to a significant diminution of naive T-cell numbers, we found impaired development of a diver
262 -specific CD8(+) T cells, but overall CD8(+) T cell numbers were either unaffected or only mildly inc
264 a.c. of TCR-transgenic OT-I mice, and CD8(+) T cell numbers were increased within eyes, suggesting th
265 ficantly protected from infection and CD4(+) T cell numbers were maintained in both the blood and the
268 tic cells decreased in blood, whereas NK and T cell numbers were only marginally altered during the c
271 but single-positive thymocyte and peripheral T cell numbers were reduced, reflecting a T cell-autonom
273 t was normal in both strains, but peripheral T cell numbers were significantly decreased in DKO mice.
276 ted and cytokine-producing CD4(+) and CD8(+) T cell numbers were still significantly reduced 1 wk lat
280 ontrol subjects, but decreases in CLA(+) TH1 T-cell numbers were greater in children with AD (17% vs
288 Both Foxp3(-) and Foxp3(+) pMHCII-specific T-cell numbers were reduced in mice expressing the antig
290 that regardless of transplant type, overall T-cell numbers were similar, although a faster rate of T
291 icient (CD45KO) mice have reduced peripheral T cell numbers where CD8 T cells are underrepresented.
292 reduction of NK cell (90% from baseline) and T-cell numbers whereas CD8 effector memory T-cell popula
293 f thymocytes and slightly reduced peripheral T cell numbers, whereas B cell-specific deletion of FADD
294 ad significantly reduced NK, NKT, and CD8(+) T cell numbers, whereas rIL-15/IL-15Ralpha restored thes
295 ad significantly increased Gag-specific CD8+ T cell numbers, whereas total cell, lymphocyte, and CD4+
296 ial thymus recovery and boosts donor-derived T cell numbers, which correlates with increased adhesion
298 sitive association of CD4(+)CD25(+) FoxP3(+) T cell numbers with allergic sensitization (P = 0.05) an
299 atous lesions, while a correlation of IL-17+ T cell numbers with tenascin C-expressing cells and MMP-
300 e of IL-10 resulted in enhancement of CD8(+) T cell numbers without detectable alterations in the kin
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