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1 elevated serum Ab concentrations elicited by primary immunization.
2 ones using whole-cell pertussis vaccines for primary immunization.
3 iarteriolar lymphoid sheath (PALS) 3 d after primary immunization.
4 a gal, which was still pronounced 5 wk after primary immunization.
5 n in all participants who were sampled after primary immunization.
6  IL-2+) were detectable within 7 days of the primary immunization.
7 E-CV booster after an inactivated JE vaccine primary immunization.
8 ses, independent of the levels measured post-primary immunization.
9 bola glycoprotein-specific IgG 28 days after primary immunization.
10 ion of memory required CD4(+) T cells during primary immunization.
11 ng periods within germinal centers following primary immunization.
12 of antigen-specific cells in the weeks after primary immunization.
13 l responses were observed 100 days after the primary immunization.
14 an be induced as early as 5-7 days following primary immunization.
15 pneumococcal challenge nearly 4 months after primary immunization.
16 t of viruses that were neutralized after the primary immunization.
17 d, but were still detectable 1 to 3 yr after primary immunization.
18 educed if anti-CD40 MAb were included in the primary immunization.
19 globulin M (IgM) to IgG1 by day 25 following primary immunization.
20 sponses following boosting at 14 weeks after primary immunization.
21 e T cells, particularly at early times after primary immunization.
22 n protein nanoparticle or "free" forms after primary immunization.
23 ce to mount a recall response 52 weeks after primary immunization.
24 a of immunized BALB/c mice 3 weeks following primary immunization.
25 phimurium-specific T-cell response following primary immunization.
26  from immune responses following a single or primary immunization.
27         Giving the anti-GITR mAb both during primary immunization and at the time of booster vaccinat
28 l tissue for humoral adaptive immunity after primary immunization and boost with a rhabdovirus, the v
29 e responses by IL-2/Ig was evident after the primary immunization and increased with subsequent boost
30 bodies are evident within several days after primary immunization and that Rad51 staining in vivo is
31 /peptide tetramer staining peaked 2 wk after primary immunization and then declined, but were still d
32                                    Following primary immunization and two boosters, high titer respon
33 centers were absent in SH2D1A(-/-) mice upon primary immunization, and because SH2D1A was detectable
34 t with anti-Hib IgG <1.0 microg/mL following primary immunization, antibody avidity after booster was
35 ce of memory B cells and plasma cells during primary immunization are not well defined.
36 >or=1:4 for serogroups C, W-135, and Y after primary immunization, as did at least 60% for serogroup
37                                    Following primary immunization, B cells differentiate to memory ce
38                           One year after the primary immunization, both groups were randomized again
39 nished serum anti-PPS14 concentrations after primary immunization but enhanced antibody responses aft
40 une responses occurs when rMVAs are given as primary immunizations but not when they are used as boos
41 tion of endogenous complement at the time of primary immunization by treatment with cobra venom facto
42 wed that 92.5% of children had completed the primary immunizations by their first birthday and 87.9%
43 ad higher frequencies of Th1 responses after primary immunization compared to all other vaccine group
44 igher than in mice that had not received the primary immunization concurrently with anti-CD40L treatm
45 resence and type of TLR adjuvant used during primary immunization conferred stability and dramaticall
46 ced whole-cell pertussis (wP) vaccine in the primary immunization course in October 2004.
47                                   During the primary immunization course, postimmunization pain on le
48 Sri Lanka succeeded in maintaining very high primary immunization coverage also but that it is feasib
49 s to the cloned immunogen 15 weeks after the primary immunization, despite preexisting immunity to th
50 formation, secondary immunization 4 wk after primary immunization did not increase NP-specific IgG.
51                                              Primary immunization enhanced TCR-V cell frequency in th
52 umoral and cellular immune responses after a primary immunization even at diluted doses.
53 y and that oral or ileal vector delivery for primary immunization facilitates the generation of mucos
54 condary immunization compared with after the primary immunization for optimal induction of Ig.
55    Mice receiving (CR2)2-IgG1 at the time of primary immunization had a marked reduction in the prima
56 tramethylpecadentane-treated mice undergoing primary immunization implicates ectopic lymphoid tissue
57  had contact with vaccinia virus since their primary immunization in early childhood.
58  evidence of increased risk of disease after primary immunization in infants whose mothers received m
59    Among children with JIA who had undergone primary immunization, MMR booster vaccination compared w
60                                    Following primary immunization, NP-specific B cells bearing V186.2
61                                              Primary immunization of 3-week-old weanling BALB/c mice
62                                 Furthermore, primary immunization of CD4(+) T cell-deficient mice wit
63                                              Primary immunization of healthy adults with vaccinia vir
64 on the relative risk (RR) of pertussis after primary immunization of infants born to vaccinated vs. u
65      CT-B administration did not inhibit the primary immunization of mice to tetanus toxoid.
66 s HA-specific IgG hybridomas generated after primary immunization of non-Tg mice was present at great
67  19 of these peptides were used for in vitro primary immunizations of PBMC derived from HLA-A11 healt
68                                         Upon primary immunization, participants with pre-existing imm
69 ere first detected in the spleen 7-8 d after primary immunization, reached peak numbers from days 10-
70 tion yielded greater efficacy than any other primary immunization route alone.
71                 The hierarchical rankings of primary immunization route with respect to efficacy were
72  booster vaccination given 4 weeks after the primary immunization series.
73   These data suggest that polysaccharide and primary immunizations should be administered prior to ri
74                        Three weeks after the primary immunization, significantly higher levels of muc
75 and differentiation of memory T cells during primary immunization suggest that a short duration betwe
76 +) and CD8(+) T cell responses 1 month after primary immunization that were comparable to those induc
77 n ibandronate was injected into mice after a primary immunization to mimic common antiosteoporotic tr
78  absence of detectable antibody titers after primary immunization, together with the rapid appearance
79 th recipients with hSBA titers >or=1:4 after primary immunization were serogroup A, 93% (84%-98%); C,
80            Salivary IgA and IgG responses to primary immunizations were generally poor.
81 d spleen, but not to GC in lymph nodes after primary immunization (where binding is dominated by vasc
82  responses to SBR were reduced following the primary immunization, whereas a compensatory role for ei
83  transient IgE Ab responses 7 days after the primary immunization, whereas no IgE Ab responses were s
84 nteers with no prior JE vaccination received primary immunization with (group 1) JE-MB or (group 2) J
85             When administered at the time of primary immunization with a vaccinia virus vector encodi
86        An immune response was observed after primary immunization with Ad26.ZEBOV; boosting by MVA-BN
87  two immunizations of RTS,S/AS01 following a primary immunization with adenovirus 35 (Ad35) (ARR) vec
88 PIV vector expressing RSV antigen to boost a primary immunization with an attenuated RSV warrants fur
89 the boost in all animals that had received a primary immunization with any of the TLR adjuvants.
90 n vaccine recipients before and 1 week after primary immunization with Aventis Pasteur smallpox vacci
91             Due to waning immunity following primary immunization with COVID-19 vaccines, booster dos
92  both Th1 and Th2 responses induced during a primary immunization with DCs, and did not reverse an ex
93                                              Primary immunization with European TBE vaccines, as reco
94  cells was significantly increased 5 d after primary immunization with G14D-CCV and at 3 d after a bo
95 ha) monoclonal antibody (MAb) at the time of primary immunization with intact Streptococcus pneumonia
96 s measured at 5 mo of age (1 mo after 3-dose primary immunization with MenC conjugate vaccine), and t
97  level, suggests that protection afforded by primary immunization with plasma-derived hepatitis B vac
98                   The protection afforded by primary immunization with plasma-derived hepatitis B vac
99 the infant humoral immune response following primary immunization with pneumococcal conjugate vaccine
100 majority of CD8 T cells do not survive after primary immunization with poly I:C and Ag, impairing mem
101  generate HA-specific B cell responses after primary immunization with PR8 virus.
102 uired only within the first 48 to 72 h after primary immunization with R36A and was induced both by n
103 We evaluated a prime-boost strategy in which primary immunization with RSV was boosted by secondary i
104                                              Primary immunization with such a multiple antigenic pept
105 immunoglobulin (Ig)G2a or IgG1 within 5 d of primary immunization with Swiss type mouse mammary tumor
106 th all-trans-RA, PIC, or both at the time of primary immunization with tetanus toxoid.
107                                   Similarly, primary immunization with the 92F strain of L. monocytog
108                                              Primary immunization with the Ad-E2 vaccine, compared to
109                                            A primary immunization with the F1 genetic vaccine followe
110 esponse to antigen were strongly enhanced by primary immunization with the fusion protein.
111 ls in an autoimmune model through the use of primary immunization with the myelin oligodendrocyte gly
112                                 For example, primary immunization with the p60 218F strain of L. mono
113   Vaccine effectiveness was calculated after primary immunization with two doses of BNT162b2 (Pfizer-
114                                              Primary immunization with two doses of ChAdOx1 nCoV-19 o
115                                   Similarly, primary immunization with unencapsulated MenC or GBS-III
116 responses from CD8(+) T cell responses after primary immunization with varying dilutions of APSV.
117 ponses to pathogen infection in humans using primary immunization with yellow fever virus (YFV) vacci

 
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