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1 letion of lmo2185 in the srtB region reduced listerial [(59) Fe]-Hn transport, and purified Lmo2185 b
2 cruited to the bacterial cell surface by the listerial ActA protein.
3 s lytic activity potentiates presentation of listerial Ags by class I MHC and inhibits presentation v
4 imilar to CD4+ T cells induced to endogenous listerial Ags.
5 he delayed-type hypersensitivity response to listerial antigen while not significantly altering cellu
6             Cross-presentation of irradiated listerial antigens to CD8(+) T cells involved TAP- and p
7                                          The listerial burden of the liver decreased 0.5 to 1.0 log,
8 stitute a significant proportion of the anti-listerial CD8+ T cell repertoire, the kinetics and magni
9     These data highlight the requirement for listerial cytoplasmic invasion for the optimal priming o
10 to a dominant MHC class II (H-2k)-restricted listerial determinant, when coinjected i.p. with murine
11 a pigs that led to the identification of 201 listerial genes important for infection of the placenta
12 ast cell culture systems were permissive for listerial growth and cell-to-cell spread and revealed th
13 ce gene expression significantly impairs the listerial growth rate (mu) and maximum growth (A) in ric
14  concentration, and the srtA-independence of listerial Hn/Hb uptake distinguished it from comparable
15             The contribution of sst1 to anti-listerial immunity is much greater in immunodeficient sc
16 quired to recruit neutrophils to the site of listerial infection in the decidua basalis, and infectio
17                            The hallmark of a listerial infection is a cell-mediated immune response t
18 cules (CD40, CD80, and CD86) were induced by listerial infection only when the bacteria invaded the c
19 in the efflux of Fe(II), and not heme during listerial infection.
20 crophages were essential to defend against a listerial infection.
21 osage leads to reduced survival of a primary listerial infection.
22 ms are operative in the context of a chronic listerial infection.
23  of CD8+ T lymphocytes in host resistance to listerial infections of the liver may be due to their ca
24 xplore the role of NK cells in resistance to listerial infections of the liver, lymphokine-activated
25 ing very early during the course of systemic listerial infections.
26 se severity (measured by lethality) and (ii) listerial infectivity (measured by liver and spleen colo
27               Episodes of community-acquired listerial meningitis confirmed by cerebrospinal fluid cu
28 ate of unfavorable outcome among adults with listerial meningitis has increased over a 14-year period
29 RB6-8C5-treated mice appeared to result from listerial multiplication in the spleen and liver rather
30 al administration of a profoundly attenuated listerial mutant can safely elicit solid protective immu
31 Gbp10--conferred cell-autonomous immunity to listerial or mycobacterial infection within macrophages
32 previously unrecognized as playing a role in listerial pathogenesis were identified: knockdowns affec
33  CD8(+) T cell hybridoma (D7) specific for a listerial peptide (LemA).
34 m-diaminopimelic acid crossbridge within the listerial peptidoglycan.
35 n, indicating its potential significance for listerial persistence in the environment and for food sa
36 cV mutation precludes the binding of certain listerial phages and produces a profound attenuation cha
37  namely that Irgm1 targets mycobacterial and listerial phagosomes.
38 Hepatocytes constitute the principal site of listerial replication in the livers of mice infected i.v
39 Tn917 insertion mutant of the mouse-virulent listerial strain F6214-1.
40                                          Two listerial strains of differing serotype (1/2a and 4nonb)
41 periments, comparable in degree to classical listerial virulence factor mutants.
42 reiterating the importance of this system in listerial virulence.

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