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1 a primary intravaginal infection and after a challenge infection.
2 mune to naive animals, confers resistance to challenge infection.
3 ng T(CD8) during heterotypic influenza virus challenge infection.
4 decreased size of the abscesses following a challenge infection.
5 double KO mice passively against P. chabaudi challenge infection.
6 nated rats also produced less total IgE upon challenge infection.
7 HeJ and outbred mice from a tick-transmitted challenge infection.
8 o confer a high degree of protection against challenge infection.
9 n the intestinal villi increased following a challenge infection.
10 onors to nonimmune recipients before vaginal challenge infection.
11 ction against nonlethal and lethal P. yoelii challenge infection.
12 emely high parasitemia and did not survive a challenge infection.
13 runcated OspA fragment can protect mice from challenge infection.
14 ina RAP-1 induced partial protection against challenge infection.
15 ficant levels of protective immunity against challenge infection.
16 n and their correlation with protection from challenge infection.
17 response, resulting in improved control of a challenge infection.
18 unocompromised mice against lethal bacterial challenge infection.
19 nhanced protection of immunized mice against challenge infection.
20 in a typical anamnestic response following a challenge infection.
21 otic-treated mice remained protected against challenge infection.
22 h during a primary infection and following a challenge infection.
23 IgM, were protected against fatal ehrlichial challenge infection.
24 of both CD4(+) and CD8(+) T cells survived a challenge infection.
25 induced potent protective immunity to lethal challenge infection.
26 vaccine conferred complete protection from a challenge infection.
27 ed to naive mice, regardless of the route of challenge infection.
28 airways of vvG-immunized mice undergoing RSV challenge infection.
29 ice were protected against lethal ehrlichial challenge infection.
30 control the level of parasitemia following a challenge infection.
31 for the cVLP group, 67% of mice survived the challenge infection.
32 nhanced antilisterial protection following a challenge infection.
33 a mouse model results in cure from a lethal challenge infection.
34 ed an unexpected role for these cells during challenge infection.
35 8-deficient mice survived secondary low-dose challenge infection.
36 ed or prevented cyst formation after type II challenge infection.
37 nse and to control growth of an airborne Mtb challenge infection.
38 he bacterial load in the lungs after aerosol challenge infection.
39 pahangi L3 protected athymic recipients from challenge infection.
40 lenge, these rapidly expanded to counter the challenge infection.
41 n correlated with antibody to MSP3 raised by challenge infection.
42 eterologous wt A/Netherlands/219/2003 (H7N7) challenge infection.
43 ferred partial protection against a virulent challenge infection.
44 e CD4 and CD8 response following primary and challenge infections.
45 ive Th1 responses that protect the mice from challenge infections.
46 SP-1) results in protection against hookworm challenge infections.
47 SP-2 provides significant protection against challenge infections.
48 ecreased CD4 T-cell recall responses against challenge infections.
49 larvae is IgM dependent for both primary and challenge infections.
50 ions of the lipoproteins protected mice from challenge infections.
51 ticing clinicians in the management of these challenging infections.
52 tested in the mouse model against homologous challenge infection after 12, 16, and 20 weeks postvacci
53 gen presentation) were not able to control a challenge infection after vaccination, indicating an ess
54 O) mice displayed reduced protection against challenge infection, although they developed a normal IF
55 ted with B. burgdorferi N40 can also prevent challenge infection and induce disease regression in inf
56 and type 1 CD8(+) T cells that expanded upon challenge infection and provided >90% control of parasit
57 o evidence of resistance to low-dose aerosol challenge infection and quickly developed severe lung da
58 against homologous and heterologous aerosol challenge infection and should be considered viable cand
59 mmittee is to advance our knowledge of these challenging infections and implement studies to improve
60 t Osp C (N40) were susceptible to tick-borne challenge infection, and nymphal ticks remained infected
61 mice provided at least partial resistance to challenge infection, and protection could also be achiev
62 P-19, protects mice against fatal ehrlichial challenge infection, and we identified a CD4 T-cell epit
65 protein-1 do not to predict protection from challenge infection but can be used as sensitive marker
66 ived IL-13 during both primary and secondary challenge infections but generate stronger canonical CD4
67 did not participate in actively killing the challenge infection, but rather were responsible for the
68 antly higher protection against intravaginal challenge infection by the HSV-2 186 strain in WT mice t
69 level of protection against wild-type virus challenge infection compared to the strain with the Q226
71 lphabeta+ CD8+ CD4- T cells, did not survive challenge infection following PAR immunization, indicati
74 d increased protection to an M. tuberculosis challenge infection; however, mice infected via the resp
77 results in persistence and immunity against challenge infection in cattle that control the initial p
78 that classical macrophage activation during challenge infection in H99gamma-immunized mice was assoc
80 duce partial, serum-transferable immunity to challenge infection in rats when administered as an alum
81 hoid tissues, and responded to and cleared a challenge infection in the complete absence of SLOs.
82 LT-2 conferred over 73% protection against a challenge infection in the jird model and over 64% prote
85 de restimulation and expanded in response to challenge infection, indicating that these cells are fun
86 B cells and T cells were unable to control a challenge infection, indicating the critical role of lym
87 g has shown that protection from a secondary challenge infection is a complex and elegant process tha
88 asite-specific mAbs or polyclonal Abs before challenge infection, it was possible to dissociate mast
89 nated monkeys were protected; thus, a single challenge infection may underestimate vaccine efficacy.
90 stently infected mice controlled a secondary challenge infection more rapidly than nonpersistently in
91 CD8 CTLs only confer protective immunity if challenge infection occurs within 48 hours of T cell inf
92 rformed with Osp C (PKo) antiserum prevented challenge infection of mice with a clone of PKo spiroche
95 face antigens of intact S2308 bacteria after challenge infection of the vaccinated mice with S2308.
97 ce provides early protection against vaginal challenge infection, probably by neutralizing virus in t
98 us ehrlichia infection, a secondary low-dose challenge infection resulted in fatal disease and loss o
99 s in S3- plus IL-12-vaccinated mice prior to challenge infection revealed a moderate elevation in imm
100 ced by increased numbers of parasites at the challenge infection site and by extensive mortality.
101 r the fifth component of complement resist a challenge infection, suggesting that neither Fc-receptor
102 of protecting the recipients from a virulent challenge infection, suggesting the emergence of T-cell
104 lungs of vaccinated mice at 2.5 weeks after challenge infection, these observations elucidate the im
105 ional changes after a secondary/systemic Xtc challenge infection; these changes were dependent on the
106 themselves do not provide any protection to challenge infection, they do reduce weight loss, lower v
107 evention, management, and treatment of these challenging infections to improve patient outcomes.
108 als as well as in humans, the possibility of challenge infection via aerosol needs to be considered t
109 ve expulsion of adult H. bakeri worms from a challenge infection was delayed in selenium (Se)-deficie
113 nical symptoms of infection after rhinovirus challenge, infection was followed by measuring antirhino
115 omoting cytokines as well as resistance to a challenge infection were suppressed by THC (8 mg/kg) inj
118 of Schistosoma mansoni display resistance to challenge infection, which increases with multiple boost
122 ally, 40% of the mice were protected against challenge infection with a lethal dose of rabies virus.
123 animals, the host T-lymphocyte response to a challenge infection with C. parvum was restricted to alp
125 d during a primary infection and a secondary challenge infection with H. polygyrus bakeri Genetic del
126 immunogenic and protected these animals from challenge infection with homologous and heterologous wil
127 the cohort immunized with BmALT-2 cleared a challenge infection with infective Brugia pahangi L3 in
128 owed significantly greater susceptibility to challenge infection with IOE compared to untreated mice
135 on with rPyMSP-1/8 failed to protect against challenge infection with reticulocyte-restricted P. yoel
136 to the development of lung eosinophilia upon challenge infection with RSV, a pathology indicative of
138 ass II-/- mice are completely protected from challenge infection with the same virus administered wit
139 ith RB51WboA were better protected against a challenge infection with the virulent strain 2308 than t
143 es are required for clearance of primary and challenge infections with B. pahangi third-stage larvae
144 s to tolerate, with reduced disease lesions, challenge infections with DC3000 and P. syringae pv. tab
145 IgE, and basophil-derived IL-4/IL-13 during challenge infections with Heligmosomoides polygyrus and
146 nst chronic T. gondii infections and against challenge infections with highly virulent tachyzoites in
148 mia, compared with levels for naive mice, in challenge infections with mixed inocula of the immunizin
149 protection (80 to 100%) following intranasal challenge infections with type 24 group A streptococci.
150 tibodies that protected mice from intranasal challenge infections with virulent group A streptococci.
151 displayed a marked increase in resistance to challenge infection, with some animals demonstrating com
152 ive activities against a lethal rabies virus challenge infection, with SPBN-Cyto c(+) revealing an ef
153 in intravaginal 50% infectious doses and in challenge infections, with the Weiss isolate displaying
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