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1 accharide (PS)-specific IgG titers following booster immunization.
2 d) were taken before and 28 days after PCV13 booster immunization.
3  CD8(+) T cell anamnestic response following booster immunization.
4 tivector antibodies did not interfere with a booster immunization.
5 obulin diversity, and cannot be corrected by booster immunization.
6  for the improved survival that results from booster immunization.
7 mediate the enhanced protection conferred by booster immunization.
8 virulent wild-type Lm without the need for a booster immunization.
9  above that seen in colonized controls after booster immunization.
10 ated to immunizing dose, and was enhanced by booster immunization.
11 n (KLH) before subcutaneous immunization and booster immunization.
12 week 18 (P < 0.001), i.e., 3 weeks after the booster immunization.
13 er, 2 of 5 animals were given an intradermal booster immunization.
14  cells for augmented IgG responses following booster immunization.
15 ugmented PS-specific IgG responses following booster immunization.
16  antibodies expected to dampen the effect of booster immunizations.
17 iming followed by recombinant fowl pox virus booster immunizations.
18 se appeared to be augmented following dermal booster immunizations.
19                                            A booster immunization 12 weeks after the prime immunizati
20 modified vaccinia virus Ankara (MVA) ME-TRAP booster immunization 8 weeks later (n = 26).
21 ypic marker CD127 and the effectiveness of a booster immunization administered early after the initia
22  low antibody titers to DEN2 and DEN3, but a booster immunization after 4 months increased the neutra
23 alized LeTx in vitro 78 days after the final booster immunization and protected the mice from in vivo
24 reached 1:10,000 immediately after the final booster immunization and then decayed to 1:150 at 6 mont
25       Animals were sacrificed 1 wk after the booster immunization, and PPs, mesenteric lymph nodes, a
26  various B cell populations, the response to booster immunization, and the generation of plasma cells
27 mmunization with G14D-CCV and at 3 d after a booster immunization as compared with control fish only
28                                            A booster immunization at week 17 after the initial immuni
29 ustained for at least 7 months following the booster immunization, at which time the secretory IgA an
30 moted entry into the brain, but a subsequent booster immunization caused a dramatic accumulation of T
31  amplification of Ag-specific CD8 T cells by booster immunization, despite an undetectable primary re
32                          A subsequent single booster immunization did not further enhance the antibod
33 rgp160 or placebo over 6 months, followed by booster immunizations every 2 months.
34        These findings support the use of ACP booster immunizations for adolescents and adults, to pro
35 tologous T cells followed by post-transplant booster immunizations improved the severe immunodeficien
36                                        After booster immunization in a rabbit, we find that the antig
37          However, although widespread use of booster immunizations in humans generates secondary and
38       Activated MBCs were also induced by TT booster immunization, indicating that the expansion of t
39 ondary expansion in response to a variety of booster immunizations, leading to elevated numbers of ef
40              These data suggest that regular booster immunizations may be required to sustain protect
41                          One primary and one booster immunization of 30 micrograms DNA per rabbit yie
42                                  In summary, booster immunization of adults with acellular pertussis
43 on and the IgG1/IgG2a ratio even following a booster immunization of KLH/CFA.
44              Also, in contrast with GBS-III, booster immunization of MenC-primed mice with isolated M
45 neous tumors, but only in combination with a booster immunization of the recipient post-BMT.
46                                              Booster immunizations of either a second dose of dendrit
47  immunizations but not when they are used as booster immunizations, suggesting that these APC-modulat
48                                      After a booster immunization, these individuals generated a robu
49  to other H5 antigen vaccines, it required a booster immunization to prime protective immune response
50 TM expansion in the presence of TE, enabling booster immunizations to bypass TE-mediated negative fee
51 ed liposome preparations required one or two booster immunizations to develop a substantial anti-AgI/
52                                  This allows booster immunizations to rapidly expand CD8(+) central m
53                                        After booster immunization, vaccinated rabbits formed no new p
54 nd whether augmented IgG responses following booster immunization were also dependent on CD4(+) T cel
55 rition of memory CD8 T cells was reversed by booster immunization, which restored protection.
56 )ICOS(+) cTfh subset clonally expanded after booster immunization whose frequencies correlated with v
57 ons with an E1-deleted Ad vector followed by booster immunization with a poxvirus vector and they sur
58 , but these T cells failed to expand after a booster immunization with a replication-defective adenov
59          A subset of participants received a booster immunization with an A/Indonesia(H5N1) vaccine a
60 IgG2a secretion upon a subsequent intranasal booster immunization with an E1-deleted adenoviral recom
61 ugmented PS-specific IgG response similar to booster immunization with intact MenC.
62 fied IgG recovered from mice 3 weeks after a booster immunization with live L3 was shown to transfer
63 immune responses were greatly enhanced after booster immunization with recombinant influenza viruses
64 antly with the DNA vaccine before intranasal booster immunization with the recombinant vaccine.
65  enhance PS-specific IgG responses following booster immunization with their encapsulated isogenic pa
66                                              Booster immunizations with Ag 21 days after the initial
67 r of chimpanzee origin allows for sequential booster immunizations with heterologous vaccine carriers
68 ike immune response to GLU after primary and booster immunizations with Salmonella expressing GLU.
69 Ad-SIV immunization, all groups received two booster immunizations with SIV gp140 and SIV Nef protein
70           Our results show that heterologous booster immunizations with the chimpanzee-derived Ad vec
71 nst heterologous R5 viruses after one or two booster immunizations with the mismatched oligomeric HIV
72 o pp65-2 cellular responses after the second booster immunization, with rapid responses observed with
73 ristics, including the ability to respond to booster immunization within days of initial priming.
74 tly, cross-primed CD8 T cells can respond to booster immunization within days of the initial immuniza

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