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1 g a significant HER-2/neu protein-specific T-cell proliferative response.
2 , that generated a low-level but clear-cut T cell proliferative response.
3 s nor everolimus could inhibit the CD4CD28 T-cell proliferative response.
4 expression was associated with an impaired T cell proliferative response.
5 cells, and elicits a robust TLR9-dependent B cell proliferative response.
6 also abolishes primary mitogen-induced liver cell proliferative response.
7 amma, TNF-alpha, and IL-6 in the augmented T cell-proliferative response.
8 ory mediators, and failed to induce robust T cell proliferative responses.
9 by significant adaptive CD4(+) and CD8(+) T cell proliferative responses.
10 ergic subjects but did not change in vitro T-cell proliferative responses.
11 e potency of APCs and boost mitogen-driven T-cell proliferative responses.
12 mia was not associated with an increase in T cell proliferative responses.
13 ted in a significant enhancement of T-helper cell proliferative responses.
14 t spleen APC in vitro leads to normal CD4+ T cell proliferative responses.
15 involved in the ability of FDC to inhibit T-cell proliferative responses.
16 er, mIEC did not inhibit splenic alphabeta T cell proliferative responses.
17 nt reduction in both MBP- and PLP-specific T cell proliferative responses.
18 or antibody binding and induction of human T-cell proliferative responses.
19 ncreasing cholesterol efflux suppressed stem cell proliferative responses.
20 ccompanied by diminished antigen-specific, T-cell proliferative responses.
21 mparable levels of IL-2 and IL-4 and similar cell proliferative responses.
22 al blood lymphocytes and better priming of T-cell proliferative responses.
23 nges paralleled reduced IL-2 secretion and T cell proliferative responses after TCR-CD28 stimulation
24 onstruct produced antibodies and exhibited T-cell proliferative responses against core or envelope.
26 ignificantly increased autoantigen-induced T cell proliferative responses along with greater numbers
27 on of innate immune responses and adaptive T cell proliferative responses, along with only transient
28 ides containing these sequences stimulated T cell proliferative responses, although less intensely th
29 ld increase in the median p24-induced CD4+ T-cell proliferative response and a 57% increase in the nu
30 of E4 and E1 had little impact on the CD4 T-cell proliferative response and cytolytic activity of CD
31 creased its effectiveness in costimulating T cell proliferative response and early IL-2 production in
33 characterized by antigen-specific impaired T cell proliferative responses and a distinct pattern of c
34 e treated with recombinant Map had reduced T cell proliferative responses and a significantly reduced
35 mpared with Ab positivity, we assessed the T-cell proliferative responses and Ab responses (islet cel
36 raft histopathology as well as anti-HLA-A2 T-cell proliferative responses and anti-HLA-A2 antibody de
38 g that anti-TNF treatment in vivo enhances T cell proliferative responses and cytokine production pro
43 insight into how TNF may inhibit endothelial cell proliferative responses and modulate angiogenesis i
44 significant levels of OVA-specific CD4(+) T cell proliferative responses and OVA-induced IFN-gamma a
45 n, significant levels of OVA-specific CD4+ T cell proliferative responses and OVA-induced IL-4 and IL
48 lsed DC can induce both E7-specific CD4(+) T-cell proliferative responses and strong CD8(+) CTL respo
51 and/or SRL both in vitro (by inhibiting of T-cell proliferative response) and in vivo (by inhibiting
52 pecific intrahepatic and peripheral CD4(+) T cell proliferative responses, and cytokines (enzyme-link
53 globulin A (IgA)- and IgG-secreting cells, T-cell proliferative responses, and gamma interferon secre
54 n of maturation markers, IL-12 production, T cell proliferative responses, and IFN-gamma production.
56 enhancement in anti-CD3-stimulated CD4(+) T-cell proliferative responses, and this proliferation was
58 llergen-driven IL-4(+) CD4(+) T cells, and T-cell proliferative responses are detectable in the perip
59 present on the surface of donor DCs, donor T cell proliferative responses are generated only in respo
62 mg/kg APAP, these changes plus a potentiated cell-proliferative response are necessary for protection
63 , protective GSH is more abundant, and where cell-proliferative responses are better able to sustain
65 n significantly increased the CEA-specific T-cell proliferative responses as well as the cytolytic T-
67 y positions induced enhanced specific CD4+ T cell proliferative responses at lower peptide concentrat
69 the regulation of activated CD4(+) T-helper cell proliferative responses; blocking this interaction
70 pe, fail to mount a detectable FV-specific T-cell proliferative response but nevertheless produce FV-
71 eneic MLRs between DCs and T cells reduced T cell proliferative responses but did so less efficiently
72 necrosis factor alpha failed to block the T cell proliferative responses, but anti-IL-2 was strongly
73 timulatory activity for primary and memory T-cell proliferative responses, but this was substantially
74 terized by a lack of virus-specific CD4(+) T-cell-proliferative responses, but strong responses have
77 e formation prior to the induction of full T cell proliferative responses by concurrent indirect Ag p
78 ory T cells that more efficiently suppress T cell proliferative responses by mixed leukocyte reaction
79 hock-protein peptides elicited significant T-cell proliferative responses by the gamma delta subset o
80 ells, B cells, or natural killer cells, or T-cell proliferative response compared with interferon bet
81 s showed enhanced suppressive activity for T cell proliferative responses compared with freshly isola
83 d activation of beta-catenin, and epithelial cell proliferative responses during C. rodentium infecti
85 kground resulted in a dramatically reduced B cell proliferative response following IgM ligation, char
86 284, 295-314, and 305-324) elicited strong T-cell proliferative responses from all strains of mice wh
87 re, both the magnitude of p24-induced CD4+ T-cell proliferative responses from CD8-depleted PBMC and
89 emonstrated CMV-specific CD4(+) and CD8(+) T cell proliferative responses from PBMC, with CD4(+)IFN-g
90 induced a rapid increase in NK activity, NK cell proliferative responses, generation of lymphokine-a
91 Our results suggest that the inhibition of T cell proliferative response in microgravity culture is a
93 ptophan (1-mT) results in increased CD4(+) T-cell proliferative response in PBMCs from HIV-infected p
95 eta fusion cells failed to induce a strong T cell proliferative response in vitro, mainly due to the
99 the CTLp frequency, anti-NP Ab titers, and T cell proliferative responses in mice that were injected
100 f-life becomes apparent during analyses of T cell proliferative responses in mice, particularly when
101 The inhibitory activity of GR1 reduced T cell proliferative responses in MLR and induced Ag-speci
102 on of cell cycle progression and sustained T cell proliferative responses in naive T cell populations
103 epitope, peptide 5 (P5), stimulates strong T cell proliferative responses in subjects with delayed (D
105 nd TILN immunization induced specific CD4+ T cell proliferative responses in the iliac lymph nodes, w
107 rally marked, but temporary suppression of T-cell proliferative responses in vitro to phytohemaggluti
108 low level of immunogenicity; (4) decreased T-cell proliferative responses in vitro, and (5) did not i
113 Human HSCs did not stimulate allogeneic T-cell proliferative response, indicating that they are no
115 ally, both internalization of CD26 and the T cell proliferative response induced by CD26-mediated cos
120 blished in male mice: ZP3 peptide-specific T cell proliferative response is reduced and AOD is absent
121 dose levels of vaccine, peptide-specific, T-cell proliferative responses (n = 3) and/or DTH response
125 ell deficiency did not significantly alter T cell proliferative response or cause a shift in the Th1/
126 nd inguinal lymph nodes, without affecting T cell proliferative responses or levels of anticollagen a
128 mmaRIIB only modestly affected initial CD4 T cell proliferative responses, suggesting that FcgammaRII
129 anergy to recall antigens and lower (<70%) T-cell proliferative responses than controls after activat
130 resulted in abrogation of hapten-specific T cell proliferative responses that correlated with dimini
131 d of infected individuals, inhibited human T cell proliferative response through interaction with the
132 dendritic cell responses (flow cytometry), T-cell proliferative responses (thymidine incorporation),
133 peptide tolerance suppressed the in vitro T cell proliferative response to AChR and its dominant alp
136 otective effect is associated with reduced T-cell proliferative response to B-(9-23) in B-(9-23)-trea
138 s little as 5 microM PAHA led to a 10-fold T cell proliferative response to chromatin in short term o
141 iency only partially reduced the naive CD8 T cell proliferative response to IL-15/IL-15Ralpha complex
142 as associated with a significantly reduced T cell proliferative response to mycobacterial Hsp65, whic
143 uction in EAE correlated with a diminished T cell proliferative response to myelin basic protein in t
147 but two patients made primary antibody and T-cell proliferative responses to a foreign antigen admini
148 lowered serum autoantibody levels, reduced T cell proliferative responses to AChR, and an expansion i
149 immunocompromised, with reduced polyclonal T cell proliferative responses to alloantigen, defined pep
150 17 receptor (R):Fc fusion protein inhibits T-cell proliferative responses to alloantigens and prolong
151 m four different colonies side-by-side for T-cell proliferative responses to an expanded panel of aut
152 ell functions including IL-2 secretion and T cell proliferative responses to CD28 plus T cell recepto
155 We compare changes in lymphocyte subsets, T cell proliferative responses to disease-associated targe
159 /- --> F1 chimeras were also able to mount T-cell proliferative responses to foreign antigens equal t
160 rst, neither APC type was able to initiate T cell proliferative responses to full-length native Topo
163 kinase proto-oncogene, reportedly modulates cell proliferative responses to growth factors, contract
166 elper lymphocytes, manifested by increased T cell proliferative responses to HIV-1 Gag and recall ant
168 ever, it has been difficult to demonstrate T cell proliferative responses to human insulin in IDDM pa
170 in, saliva IgA binding to insulin, or CD4+ T-cell proliferative responses to insulin were observed in
172 of 25 tested persons made antigen-specific T cell proliferative responses to L2E7, and peripheral blo
174 fter the transplantation of thymus tissue, T-cell proliferative responses to mitogens developed in fo
176 L-12 significantly increased PBMC and CD4+ T cell proliferative responses to p24 Ag in HIV-infected,
180 oavailability facilitated the induction of T cell proliferative responses to suboptimal stimuli.
182 acrophages and DCs directly regulate human B-cell proliferative responses to T-cell-independent stimu
184 Eleven of the 21 patients also developed T cell proliferative responses to the homologous self-Ag.
187 s, inhibition of SIV replication, and CD4+ T cell proliferative responses to three of the extracellul
189 w also had a reduced capacity to stimulate T cell proliferative responses to tubercle bacillus Ag 85.
190 lidated linear discriminant analysis using T cell proliferative responses to two regions of Tri r 2 (
191 munization, respectively), in increases in T cell-proliferative response to HPV-16 L1 VLPs (P<.001).
192 rosis, but had no inhibitory effect on the T cell-proliferative response to myelin basic protein (MBP
194 nt than untreated DCs in driving syngeneic T cell-proliferative responses to staphylococcal enterotox
195 detected by inhibition of the Ag-specific T cell proliferative response upon Ag presentation by IFN-
197 ability to transduce CLL cells, a vigorous T-cell proliferative response was obtained using cells tra
198 endritic cells (DCs) to induce Ag-specific T cell proliferative responses was significantly reduced c
199 ed subsets of lymphocytes and quantitative T-cell proliferative response were assessed in an explorat
200 ti-IgM- and anti-CD40 plus anti-Ig-induced B cell proliferative responses were decreased in BXD2-Aicd
201 r neutralizing antibodies nor SIV-specific T-cell proliferative responses were detectable in any of t
202 ll as anti-HLA-A2 antibody development and T cell proliferative responses were determined at days +5,
203 delayed-type hypersensitivity and splenic T cell proliferative responses were examined, Peyer's patc
204 V core epitopes; however, the humoral and Th cell proliferative responses were found to be weak.
205 oy islet tissue in vivo though spontaneous T-cell proliferative responses were observed in prediabeti
206 rsistent, and vigorous HIV-1-specific CD4+ T cell proliferative responses were present, resulting in
208 Furthermore, specific CD4(+) and CD8(+) T cell proliferative responses were significantly increase
210 a significant increase in PBLs, but T and B cell-proliferative responses were not consistently enhan
211 ture DCs were used to stimulate allogeneic T cells, proliferative responses were dampened (approximat
212 sole class II molecule generated a robust T cell-proliferative response when primed with peptide 2 o
213 newborn blood specimens tested also showed T cell proliferative responses, which included a marked ex
214 h specific impairment of ex vivo antidonor T cell proliferative responses, which was not reversed by
215 These data suggest that Ply induces CD4 T cell proliferative responses with production of IFN- gam
216 e absence of strong HIV-1-specific, CD4(+) T-cell-proliferative responses, yet the mechanism underlyi
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