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1 R. conorii infection induced maturation of BMDCs from bo
2 R. conorii infection induced phosphorylation of STAT1 on
3 R. conorii, the causative agent of Mediterranean spotted
4 x (MHC) class I-matched CTL activity against R. conorii-infected SVEC-10 endothelial cells, with peak
6 s, Fc-dependent antibodies protected against R. conorii infection of endothelium and macrophages by o
10 euse fever, due to Rickettsia rickettsii and R. conorii, respectively, are characterized by widesprea
11 prowazekii genome, relative to R. typhi and R. conorii, which appears to have occurred after the typ
12 44) and OmpB(739-848) stimulated immune anti-R. conorii CD8 T lymphocytes, suggesting the presence of
13 or lipopolysaccharide (LPS), polyclonal anti-R. conorii serum, Fab fragments of polyclonal antiserum,
14 absence of particular neutralizing antibody, R. conorii is resistant to the effects of serum compleme
17 infection resulted in significantly enhanced R. conorii replication, whereas addition of exogenous IF
20 transcriptional riboregulatory mechanisms in R. conorii and interactions between a novel Rc_sR and it
21 rowazekii and R. typhi, 15 are found only in R. conorii and R. typhi, and 24 are unique to R. typhi.
22 er group (SFG) Rickettsia species, including R. conorii and R. rickettsii, is acutely dependent on ad
23 (s) because tetracycline treatment inhibited R. conorii replication, IFN-beta expression, and STAT1 p
26 ice that had been infected with 10 LD(50) of R. conorii 4 or 5 days earlier prolonged the life of the
29 ed in the development of large aggregates of R. conorii antigens in splenic macrophages and intraphag
30 ytes protected mice against a lethal dose of R. conorii in the disseminated endothelial target model.
31 e infected with lethal or sublethal doses of R. conorii by a combination of quantitative real-time po
33 At 0 h, Fc-dependent antibody enhancement of R. conorii adherence to endothelial and macrophage-like
34 monoclonal antibody inhibited the escape of R. conorii from the phagosome, resulting in intraphagoly
35 peroxide-dependent intracellular killing of R. conorii was demonstrated in HUVECs, THP-1 cells (huma
36 determined the transcriptional landscape of R. conorii during infection of Human Microvascular Endot
37 n system, we demonstrated that production of R. conorii Sca1 in the Escherichia coli outer membrane i
38 of factor H from normal human serum renders R. conorii more susceptible to C3 and membrane attack co
39 ffeensis, E. ewingii, Rickettsia rickettsii, R. conorii, and other spotted fever group rickettsiae.
41 terranean spotted fever, we demonstrate that R. conorii(pRam18dRGA[AmTrCh]) elicits the same fatal ou
43 The kinetics of development of antibodies to R. conorii determined by immunoblotting revealed antibod
49 acrophage-like cell lines were infected with R. conorii that had been exposed to polyclonal antibodie
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