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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.
25                           The frequency of T-cell proliferative responses against VP2 was significant
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
32                       The in vitro splenic T cell proliferative response and induction of IFN-gamma t
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
37                                    Primary T cell proliferative responses and cytokine production (in
38 g that anti-TNF treatment in vivo enhances T cell proliferative responses and cytokine production pro
39                                            B-cell proliferative responses and differentiation to immu
40              Allogeneic C3H/HeJ (C3H; H2k) T-cell proliferative responses and generation of cytotoxic
41                                            T-cell proliferative responses and immunoglobulin G antibo
42 ration of T-regulatory cells that suppress T-cell proliferative responses and induce tolerance.
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
46          In the mucosa, both Peyer's patch T cell proliferative responses and OVA-specific fecal IgA
47                              In contrast, Th cell proliferative responses and secretion of cytokines
48 lsed DC can induce both E7-specific CD4(+) T-cell proliferative responses and strong CD8(+) CTL respo
49               Ex vivo grass antigen-driven T-cell proliferative responses and the frequency of IL-4(+
50       Although we found both a high CD4(+) T cell-proliferative response and TH2 cytokines production
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.
55         They elicited only weak allogeneic T-cell proliferative responses, and repeated stimulation i
56  enhancement in anti-CD3-stimulated CD4(+) T-cell proliferative responses, and this proliferation was
57             The results suggest that HHV-8 T cell proliferative responses are common in HIV-negative
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
60                                            T-cell proliferative responses are inhibited during the er
61                        HIV-1-specific CD4+ T cell proliferative responses are not measurable in most
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
64                      The CD4+ inflammatory T cell proliferative responses as well as CD8+ CTL activit
65 n significantly increased the CEA-specific T-cell proliferative responses as well as the cytolytic T-
66 as negatively associated with HBV-specific T-cell proliferative responses at both time points.
67 y positions induced enhanced specific CD4+ T cell proliferative responses at lower peptide concentrat
68                  Despite a compensatory beta-cell proliferative response, beta-cell mass progressivel
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
75 monocyte (MO) cultures inhibited mitogenic T cell proliferative responses by > 95%.
76                      Suppression of CD4(+) T cell proliferative responses by both CD25(+) and CD25(-)
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
82                        H/K ATPase-specific T cell proliferative responses could first be detected 5 w
83 d activation of beta-catenin, and epithelial cell proliferative responses during C. rodentium infecti
84                             Suppression of T cell-proliferative responses during malaria has been att
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
88                     These p24-induced CD4+ T-cell proliferative responses from CD8-depleted PBMC were
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
92  of GFAP filament assembly and inhibition of cell proliferative response in Muller glia.
93 ptophan (1-mT) results in increased CD4(+) T-cell proliferative response in PBMCs from HIV-infected p
94  developmental abnormality in the epithelial cell proliferative response in those mice.
95 eta fusion cells failed to induce a strong T cell proliferative response in vitro, mainly due to the
96       Interestingly, most HCV-specific CD4 T-cell proliferative responses in AA patients were unaccom
97                   HIV-1 Ag-specific CD4(+) T cell proliferative responses in human subjects with adva
98                                            T-cell proliferative responses in individuals older than 1
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
104 rtial BAFF neutralization rescues aberrant B cell proliferative responses in such mice.
105 nd TILN immunization induced specific CD4+ T cell proliferative responses in the iliac lymph nodes, w
106     The peptide also induced LT-B-specific T-cell proliferative responses in these mice.
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
109             Like C1q, HCV core can inhibit T-cell proliferative responses in vitro.
110 sing of DC to efficiently trigger specific T-cell proliferative responses in vitro.
111 ce to generate secondary anti-VSV CTL and Th cell proliferative responses in vitro.
112 nization with this construct elicited CD4+ T cell proliferative responses in vivo.
113    Human HSCs did not stimulate allogeneic T-cell proliferative response, indicating that they are no
114                                     CD4(+) T-cell proliferative responses indicative of breakdown of
115 ally, both internalization of CD26 and the T cell proliferative response induced by CD26-mediated cos
116                           CMX-13 inhibited T cell proliferative responses induced by Con A and alloan
117                       The peripheral blood T cell proliferative responses induced by topo I and in vi
118                                   However, B cell-proliferative responses induced by stimulation of t
119          The results suggest that a strong T-cell proliferative response is induced upon rechallenge
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
122                 Peripheral blood mononuclear cell proliferative responses of 25 controls and 10 patie
123                                            T cell proliferative responses of B6.129S1-IL-12rb2(tm1Jm)
124                           In contrast with B cells, proliferative responses of CD44(hi) CD8(+) cells
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
127                  The prevention of a myeloma cell proliferative response resulting from inhibition of
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
134                           In addition, the T-cell proliferative response to allogeneic LC-derived mDC
135 f T-cell tolerance was assessed by splenic T-cell proliferative response to antigen at 5 weeks.
136 otective effect is associated with reduced T-cell proliferative response to B-(9-23) in B-(9-23)-trea
137 wild-type C57BL/6 mice and had an enhanced T cell proliferative response to bovine CII.
138 s little as 5 microM PAHA led to a 10-fold T cell proliferative response to chromatin in short term o
139                                        The T-cell proliferative response to HBcAg did not differ betw
140 ne viral load or CD4+ T cell count and the T cell proliferative response to HIV-1 Gag.
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
144 cted with T. gondii developed a gammadelta T cell proliferative response to parasite Ag.
145 RS-1 nor IRS-2 overexpression induced a beta-cell proliferative response to TGF-alpha/EGF.
146 cretion and were unable to induce a normal T cell proliferative response to TT.
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
153             Assays were performed to study T cell proliferative responses to CII in peripheral blood
154                                            T cell proliferative responses to diabetes-associated Ags
155  We compare changes in lymphocyte subsets, T cell proliferative responses to disease-associated targe
156 iltration into grafts but not with altered T-cell proliferative responses to donor stimulators.
157                      The induction of CD4+ T cell proliferative responses to eight synthetic peptides
158 iding sufficient help to allow optimal CD8 T cell proliferative responses to exosomal protein.
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
161                                  The human T cell proliferative responses to GA were HLA class II DR-
162 nd untreated MS patients exhibit prominent T cell proliferative responses to GA.
163  kinase proto-oncogene, reportedly modulates cell proliferative responses to growth factors, contract
164                                            T-cell proliferative responses to HER-2/neu peptides and i
165            It has been suggested that CD4+ T cell proliferative responses to HIV p24 Ag may be import
166 elper lymphocytes, manifested by increased T cell proliferative responses to HIV-1 Gag and recall ant
167                                 A range of T-cell proliferative responses to HPV-11 VLP were observed
168 ever, it has been difficult to demonstrate T cell proliferative responses to human insulin in IDDM pa
169           Their peripheral blood mononuclear cell proliferative responses to immunogen stimulation 4
170 in, saliva IgA binding to insulin, or CD4+ T-cell proliferative responses to insulin were observed in
171 nd saliva IgA binding to insulin, and CD4+ T-cell proliferative responses to insulin.
172 of 25 tested persons made antigen-specific T cell proliferative responses to L2E7, and peripheral blo
173                                            B-cell proliferative responses to lipopolysaccharide were
174 fter the transplantation of thymus tissue, T-cell proliferative responses to mitogens developed in fo
175                  All 7 survivors developed T-cell proliferative responses to mitogens of more than 10
176 L-12 significantly increased PBMC and CD4+ T cell proliferative responses to p24 Ag in HIV-infected,
177                                            T cell proliferative responses to purified HHV-8 were meas
178                                            T-cell proliferative responses to SIV gp140 and T-helper e
179 granule precursor cells and enhances granule cell proliferative responses to Sonic hedgehog.
180 oavailability facilitated the induction of T cell proliferative responses to suboptimal stimuli.
181                                            T-cell proliferative responses to synthetic peptides demon
182 acrophages and DCs directly regulate human B-cell proliferative responses to T-cell-independent stimu
183                                    Primary T cell proliferative responses to TCR ligation plus CD28 c
184   Eleven of the 21 patients also developed T cell proliferative responses to the homologous self-Ag.
185                                        CD4 T cell proliferative responses to the pneumococcal protein
186          Considerable heterogeneity in the T-cell proliferative responses to these three variant anti
187 s, inhibition of SIV replication, and CD4+ T cell proliferative responses to three of the extracellul
188                                            T cell proliferative responses to topo I were detected in
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
193                                            T cell-proliferative responses to a single epitope, HEL47-
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-
196 lity to enhance anti-CD3-stimulated CD4(+) T cell proliferative responses via B7-1 and B7-2.
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
207                                            T cell proliferative responses were seen with all encephal
208    Furthermore, specific CD4(+) and CD8(+) T cell proliferative responses were significantly increase
209             In these animals, MOG-specific T cell proliferative responses were transiently suppressed
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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