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1 onses and drived protection against parasite challenge infection.
2 ice were protected against virulent L. major challenge infection.
3 ferred partial protection against a virulent challenge infection.
4 a primary intravaginal infection and after a challenge infection.
5 mune to naive animals, confers resistance to challenge infection.
6 decreased size of the abscesses following a challenge infection.
7 double KO mice passively against P. chabaudi challenge infection.
8 nated rats also produced less total IgE upon challenge infection.
9 HeJ and outbred mice from a tick-transmitted challenge infection.
10 o confer a high degree of protection against challenge infection.
11 of both CD4(+) and CD8(+) T cells survived a challenge infection.
12 n the intestinal villi increased following a challenge infection.
13 onors to nonimmune recipients before vaginal challenge infection.
14 ice were protected against lethal ehrlichial challenge infection.
15 ction against nonlethal and lethal P. yoelii challenge infection.
16 emely high parasitemia and did not survive a challenge infection.
17 runcated OspA fragment can protect mice from challenge infection.
18 ina RAP-1 induced partial protection against challenge infection.
19 ficant levels of protective immunity against challenge infection.
20 th no detectable viral shedding after repeat challenge infection.
21 ce substantial protection against sporozoite challenge infection.
22 ed or prevented cyst formation after type II challenge infection.
23 DCs from WT mice, were not protected against challenge infection.
24 eterologous wt A/Netherlands/219/2003 (H7N7) challenge infection.
25 ng T(CD8) during heterotypic influenza virus challenge infection.
26 n and their correlation with protection from challenge infection.
27 response, resulting in improved control of a challenge infection.
28 ted to early plasmablast responses following challenge infection.
29 unocompromised mice against lethal bacterial challenge infection.
30 nhanced protection of immunized mice against challenge infection.
31 in a typical anamnestic response following a challenge infection.
32 otic-treated mice remained protected against challenge infection.
33 h during a primary infection and following a challenge infection.
34 IgM, were protected against fatal ehrlichial challenge infection.
35 induced potent protective immunity to lethal challenge infection.
36 vaccine conferred complete protection from a challenge infection.
37 ed to naive mice, regardless of the route of challenge infection.
38 airways of vvG-immunized mice undergoing RSV challenge infection.
39 control the level of parasitemia following a challenge infection.
40 for the cVLP group, 67% of mice survived the challenge infection.
41 nhanced antilisterial protection following a challenge infection.
42 a mouse model results in cure from a lethal challenge infection.
43 ed an unexpected role for these cells during challenge infection.
44 8-deficient mice survived secondary low-dose challenge infection.
45 nse and to control growth of an airborne Mtb challenge infection.
46 he bacterial load in the lungs after aerosol challenge infection.
47 pahangi L3 protected athymic recipients from challenge infection.
48 lenge, these rapidly expanded to counter the challenge infection.
49 n correlated with antibody to MSP3 raised by challenge infection.
50 e CD4 and CD8 response following primary and challenge infections.
51 ive Th1 responses that protect the mice from challenge infections.
52 SP-1) results in protection against hookworm challenge infections.
53 SP-2 provides significant protection against challenge infections.
54 ecreased CD4 T-cell recall responses against challenge infections.
55 larvae is IgM dependent for both primary and challenge infections.
56 ions of the lipoproteins protected mice from challenge infections.
57 ticing clinicians in the management of these challenging infections.
58 to significant advances in the treatment of challenging infections.
59 ve changed the treatment landscape for these challenging infections.
60 ritize therapeutic strategies for addressing challenging infections.
61 tested in the mouse model against homologous challenge infection after 12, 16, and 20 weeks postvacci
62 gen presentation) were not able to control a challenge infection after vaccination, indicating an ess
63 O) mice displayed reduced protection against challenge infection, although they developed a normal IF
64 ted with B. burgdorferi N40 can also prevent challenge infection and induce disease regression in inf
65 ice resulted in potent immune responses upon challenge infection and protected from disease and sever
66 and type 1 CD8(+) T cells that expanded upon challenge infection and provided >90% control of parasit
67 o evidence of resistance to low-dose aerosol challenge infection and quickly developed severe lung da
68 against homologous and heterologous aerosol challenge infection and should be considered viable cand
69 mmittee is to advance our knowledge of these challenging infections and implement studies to improve
70 ad EHV-1-specific IgG4/7 antibodies prior to challenge infection, and intranasal antibodies increased
71 t Osp C (N40) were susceptible to tick-borne challenge infection, and nymphal ticks remained infected
72 mice provided at least partial resistance to challenge infection, and protection could also be achiev
73 P-19, protects mice against fatal ehrlichial challenge infection, and we identified a CD4 T-cell epit
74 Ab4, respectively, were fully protected from challenge infection as indicated by the absence of fever
77 protein-1 do not to predict protection from challenge infection but can be used as sensitive marker
78 ived IL-13 during both primary and secondary challenge infections but generate stronger canonical CD4
79 did not participate in actively killing the challenge infection, but rather were responsible for the
80 antly higher protection against intravaginal challenge infection by the HSV-2 186 strain in WT mice t
81 level of protection against wild-type virus challenge infection compared to the strain with the Q226
84 lphabeta+ CD8+ CD4- T cells, did not survive challenge infection following PAR immunization, indicati
89 d increased protection to an M. tuberculosis challenge infection; however, mice infected via the resp
92 results in persistence and immunity against challenge infection in cattle that control the initial p
93 ction from virus shedding and viremia during challenge infection in combination with reduced virulenc
94 that classical macrophage activation during challenge infection in H99gamma-immunized mice was assoc
96 duce partial, serum-transferable immunity to challenge infection in rats when administered as an alum
97 hoid tissues, and responded to and cleared a challenge infection in the complete absence of SLOs.
98 LT-2 conferred over 73% protection against a challenge infection in the jird model and over 64% prote
99 CoV-2 ancestral WA1 strain and alpha variant challenge infection in the respiratory tracts as demonst
100 protection against a heterologous H1N1 virus challenge infection in the upper respiratory tract.
103 de restimulation and expanded in response to challenge infection, indicating that these cells are fun
104 B cells and T cells were unable to control a challenge infection, indicating the critical role of lym
105 g has shown that protection from a secondary challenge infection is a complex and elegant process tha
106 asite-specific mAbs or polyclonal Abs before challenge infection, it was possible to dissociate mast
107 nated monkeys were protected; thus, a single challenge infection may underestimate vaccine efficacy.
108 stently infected mice controlled a secondary challenge infection more rapidly than nonpersistently in
109 CD8 CTLs only confer protective immunity if challenge infection occurs within 48 hours of T cell inf
110 rformed with Osp C (PKo) antiserum prevented challenge infection of mice with a clone of PKo spiroche
113 face antigens of intact S2308 bacteria after challenge infection of the vaccinated mice with S2308.
115 ce provides early protection against vaginal challenge infection, probably by neutralizing virus in t
116 us ehrlichia infection, a secondary low-dose challenge infection resulted in fatal disease and loss o
117 s in S3- plus IL-12-vaccinated mice prior to challenge infection revealed a moderate elevation in imm
118 ced by increased numbers of parasites at the challenge infection site and by extensive mortality.
119 nduction of broadly neutralising antibodies, challenging infections such as HIV-1 could require paral
120 r the fifth component of complement resist a challenge infection, suggesting that neither Fc-receptor
121 of protecting the recipients from a virulent challenge infection, suggesting the emergence of T-cell
123 lungs of vaccinated mice at 2.5 weeks after challenge infection, these observations elucidate the im
124 ional changes after a secondary/systemic Xtc challenge infection; these changes were dependent on the
125 themselves do not provide any protection to challenge infection, they do reduce weight loss, lower v
126 owever, all seven protected mice from lethal challenge infection through their NA inhibition activity
127 evention, management, and treatment of these challenging infections to improve patient outcomes.
128 als as well as in humans, the possibility of challenge infection via aerosol needs to be considered t
129 ve expulsion of adult H. bakeri worms from a challenge infection was delayed in selenium (Se)-deficie
133 nical symptoms of infection after rhinovirus challenge, infection was followed by measuring antirhino
134 shedding was significantly reduced following challenge, infection was transmissible to susceptible co
136 omoting cytokines as well as resistance to a challenge infection were suppressed by THC (8 mg/kg) inj
139 of Schistosoma mansoni display resistance to challenge infection, which increases with multiple boost
143 ally, 40% of the mice were protected against challenge infection with a lethal dose of rabies virus.
144 animals, the host T-lymphocyte response to a challenge infection with C. parvum was restricted to alp
146 d during a primary infection and a secondary challenge infection with H. polygyrus bakeri Genetic del
147 immunogenic and protected these animals from challenge infection with homologous and heterologous wil
148 the cohort immunized with BmALT-2 cleared a challenge infection with infective Brugia pahangi L3 in
149 owed significantly greater susceptibility to challenge infection with IOE compared to untreated mice
156 on with rPyMSP-1/8 failed to protect against challenge infection with reticulocyte-restricted P. yoel
157 to the development of lung eosinophilia upon challenge infection with RSV, a pathology indicative of
159 ass II-/- mice are completely protected from challenge infection with the same virus administered wit
160 ith RB51WboA were better protected against a challenge infection with the virulent strain 2308 than t
164 es are required for clearance of primary and challenge infections with B. pahangi third-stage larvae
165 s to tolerate, with reduced disease lesions, challenge infections with DC3000 and P. syringae pv. tab
166 IgE, and basophil-derived IL-4/IL-13 during challenge infections with Heligmosomoides polygyrus and
167 nst chronic T. gondii infections and against challenge infections with highly virulent tachyzoites in
169 mia, compared with levels for naive mice, in challenge infections with mixed inocula of the immunizin
170 protection (80 to 100%) following intranasal challenge infections with type 24 group A streptococci.
171 tibodies that protected mice from intranasal challenge infections with virulent group A streptococci.
172 displayed a marked increase in resistance to challenge infection, with some animals demonstrating com
173 ive activities against a lethal rabies virus challenge infection, with SPBN-Cyto c(+) revealing an ef
174 in intravaginal 50% infectious doses and in challenge infections, with the Weiss isolate displaying