ライフサイエンスコーパス: primary immunization

1 E-CV booster after an inactivated JE vaccine primary immunization.

2 ng periods within germinal centers following primary immunization.

3 of antigen-specific cells in the weeks after primary immunization.

4 l responses were observed 100 days after the primary immunization.

5 an be induced as early as 5-7 days following primary immunization.

6 pneumococcal challenge nearly 4 months after primary immunization.

7 t of viruses that were neutralized after the primary immunization.

8 d, but were still detectable 1 to 3 yr after primary immunization.

9 educed if anti-CD40 MAb were included in the primary immunization.

10 bola glycoprotein-specific IgG 28 days after primary immunization.

11 globulin M (IgM) to IgG1 by day 25 following primary immunization.

12 sponses following boosting at 14 weeks after primary immunization.

13 e T cells, particularly at early times after primary immunization.

14 ce to mount a recall response 52 weeks after primary immunization.

15 a of immunized BALB/c mice 3 weeks following primary immunization.

16 phimurium-specific T-cell response following primary immunization.

17 from immune responses following a single or primary immunization.

18 ion of memory required CD4(+) T cells during primary immunization.

19 iarteriolar lymphoid sheath (PALS) 3 d after primary immunization.

20 a gal, which was still pronounced 5 wk after primary immunization.

21 Giving the anti-GITR mAb both during primary immunization and at the time of booster vaccinat

22 e responses by IL-2/Ig was evident after the primary immunization and increased with subsequent boost

23 bodies are evident within several days after primary immunization and that Rad51 staining in vivo is

24 /peptide tetramer staining peaked 2 wk after primary immunization and then declined, but were still d

25 Following primary immunization and two boosters, high titer respon

26 centers were absent in SH2D1A(-/-) mice upon primary immunization, and because SH2D1A was detectable

27 t with anti-Hib IgG <1.0 microg/mL following primary immunization, antibody avidity after booster was

28 ce of memory B cells and plasma cells during primary immunization are not well defined.

29 >or=1:4 for serogroups C, W-135, and Y after primary immunization, as did at least 60% for serogroup

30 Following primary immunization, B cells differentiate to memory ce

31 One year after the primary immunization, both groups were randomized again

32 nished serum anti-PPS14 concentrations after primary immunization but enhanced antibody responses aft

33 une responses occurs when rMVAs are given as primary immunizations but not when they are used as boos

34 tion of endogenous complement at the time of primary immunization by treatment with cobra venom facto

35 ad higher frequencies of Th1 responses after primary immunization compared to all other vaccine group

36 igher than in mice that had not received the primary immunization concurrently with anti-CD40L treatm

37 resence and type of TLR adjuvant used during primary immunization conferred stability and dramaticall

38 During the primary immunization course, postimmunization pain on le

39 s to the cloned immunogen 15 weeks after the primary immunization, despite preexisting immunity to th

40 Primary immunization enhanced TCR-V cell frequency in th

41 umoral and cellular immune responses after a primary immunization even at diluted doses.

42 y and that oral or ileal vector delivery for primary immunization facilitates the generation of mucos

43 condary immunization compared with after the primary immunization for optimal induction of Ig.

44 Mice receiving (CR2)2-IgG1 at the time of primary immunization had a marked reduction in the prima

45 tramethylpecadentane-treated mice undergoing primary immunization implicates ectopic lymphoid tissue

46 had contact with vaccinia virus since their primary immunization in early childhood.

47 evidence of increased risk of disease after primary immunization in infants whose mothers received m

48 Among children with JIA who had undergone primary immunization, MMR booster vaccination compared w

49 Following primary immunization, NP-specific B cells bearing V186.2

50 Primary immunization of 3-week-old weanling BALB/c mice

51 Furthermore, primary immunization of CD4(+) T cell-deficient mice wit

52 Primary immunization of healthy adults with vaccinia vir

53 CT-B administration did not inhibit the primary immunization of mice to tetanus toxoid.

54 s HA-specific IgG hybridomas generated after primary immunization of non-Tg mice was present at great

55 19 of these peptides were used for in vitro primary immunizations of PBMC derived from HLA-A11 healt

56 ere first detected in the spleen 7-8 d after primary immunization, reached peak numbers from days 10-

57 tion yielded greater efficacy than any other primary immunization route alone.

58 The hierarchical rankings of primary immunization route with respect to efficacy were

59 booster vaccination given 4 weeks after the primary immunization series.

60 These data suggest that polysaccharide and primary immunizations should be administered prior to ri

61 Three weeks after the primary immunization, significantly higher levels of muc

62 and differentiation of memory T cells during primary immunization suggest that a short duration betwe

63 +) and CD8(+) T cell responses 1 month after primary immunization that were comparable to those induc

64 n ibandronate was injected into mice after a primary immunization to mimic common antiosteoporotic tr

65 absence of detectable antibody titers after primary immunization, together with the rapid appearance

66 th recipients with hSBA titers >or=1:4 after primary immunization were serogroup A, 93% (84%-98%); C,

67 Salivary IgA and IgG responses to primary immunizations were generally poor.

68 d spleen, but not to GC in lymph nodes after primary immunization (where binding is dominated by vasc

69 responses to SBR were reduced following the primary immunization, whereas a compensatory role for ei

70 transient IgE Ab responses 7 days after the primary immunization, whereas no IgE Ab responses were s

71 nteers with no prior JE vaccination received primary immunization with (group 1) JE-MB or (group 2) J

72 When administered at the time of primary immunization with a vaccinia virus vector encodi

73 An immune response was observed after primary immunization with Ad26.ZEBOV; boosting by MVA-BN

74 two immunizations of RTS,S/AS01 following a primary immunization with adenovirus 35 (Ad35) (ARR) vec

75 the boost in all animals that had received a primary immunization with any of the TLR adjuvants.

76 n vaccine recipients before and 1 week after primary immunization with Aventis Pasteur smallpox vacci

77 both Th1 and Th2 responses induced during a primary immunization with DCs, and did not reverse an ex

78 cells was significantly increased 5 d after primary immunization with G14D-CCV and at 3 d after a bo

79 ha) monoclonal antibody (MAb) at the time of primary immunization with intact Streptococcus pneumonia

80 s measured at 5 mo of age (1 mo after 3-dose primary immunization with MenC conjugate vaccine), and t

81 level, suggests that protection afforded by primary immunization with plasma-derived hepatitis B vac

82 The protection afforded by primary immunization with plasma-derived hepatitis B vac

83 majority of CD8 T cells do not survive after primary immunization with poly I:C and Ag, impairing mem

84 generate HA-specific B cell responses after primary immunization with PR8 virus.

85 uired only within the first 48 to 72 h after primary immunization with R36A and was induced both by n

86 Primary immunization with such a multiple antigenic pept

87 immunoglobulin (Ig)G2a or IgG1 within 5 d of primary immunization with Swiss type mouse mammary tumor

88 th all-trans-RA, PIC, or both at the time of primary immunization with tetanus toxoid.

89 Similarly, primary immunization with the 92F strain of L. monocytog

90 Primary immunization with the Ad-E2 vaccine, compared to

91 A primary immunization with the F1 genetic vaccine followe

92 esponse to antigen were strongly enhanced by primary immunization with the fusion protein.

93 ls in an autoimmune model through the use of primary immunization with the myelin oligodendrocyte gly

94 For example, primary immunization with the p60 218F strain of L. mono

95 Similarly, primary immunization with unencapsulated MenC or GBS-III

96 responses from CD8(+) T cell responses after primary immunization with varying dilutions of APSV.