ライフサイエンスコーパス: R. conorii

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

5 8 lymphocytes failed to protect mice against R. conorii.

6 s, Fc-dependent antibodies protected against R. conorii infection of endothelium and macrophages by o

7 f replication, compared to R. prowazekii and R. conorii.

8 , in R. typhi, compared to R. prowazekii and R. conorii.

9 kettsial genome sequences: R. prowazekii and R. conorii.

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

15 mbinant Sca1 peptide with host cells blocked R. conorii cell association.

16 luble Sca2 protein is capable of diminishing R. conorii invasion of cultured mammalian cells.

17 infection resulted in significantly enhanced R. conorii replication, whereas addition of exogenous IF

18 prowazekii and R. typhi) and spotted fever (R. conorii) groups diverged.

19 owever, no such correlation was observed for R. conorii and R. honei.

20 es, is actively transcribed and expressed in R. conorii cells.

21 transcriptional riboregulatory mechanisms in R. conorii and interactions between a novel Rc_sR and it

22 rowazekii and R. typhi, 15 are found only in R. conorii and R. typhi, and 24 are unique to R. typhi.

23 er group (SFG) Rickettsia species, including R. conorii and R. rickettsii, is acutely dependent on ad

24 (s) because tetracycline treatment inhibited R. conorii replication, IFN-beta expression, and STAT1 p

25 tective role for STAT1 against intracellular R. conorii replication.

26 a from a mouse model of sublethal and lethal R. conorii identified RC0497 in the blood, and its circu

27 l culture similar to those of nontransformed R. conorii.

28 ice that had been infected with 10 LD(50) of R. conorii 4 or 5 days earlier prolonged the life of the

29 h later with 10 50% lethal doses (LD(50)) of R. conorii.

30 nd that Sca1 is involved in the adherence of R. conorii to host cells.

31 ed in the development of large aggregates of R. conorii antigens in splenic macrophages and intraphag

32 ytes protected mice against a lethal dose of R. conorii in the disseminated endothelial target model.

33 e infected with lethal or sublethal doses of R. conorii by a combination of quantitative real-time po

34 We investigated the effects of R. conorii infection on the status of the Janus kinase (

35 At 0 h, Fc-dependent antibody enhancement of R. conorii adherence to endothelial and macrophage-like

36 monoclonal antibody inhibited the escape of R. conorii from the phagosome, resulting in intraphagoly

37 peroxide-dependent intracellular killing of R. conorii was demonstrated in HUVECs, THP-1 cells (huma

38 determined the transcriptional landscape of R. conorii during infection of Human Microvascular Endot

39 n system, we demonstrated that production of R. conorii Sca1 in the Escherichia coli outer membrane i

40 of factor H from normal human serum renders R. conorii more susceptible to C3 and membrane attack co

41 ffeensis, E. ewingii, Rickettsia rickettsii, R. conorii, and other spotted fever group rickettsiae.

42 (+) T regulatory cells promoted by syngeneic R. conorii-infected BMDCs in the presence of IL-2.

43 terranean spotted fever, we demonstrate that R. conorii(pRam18dRGA[AmTrCh]) elicits the same fatal ou

44 We demonstrate here that R. conorii specifically interacts with the soluble host

45 whose abundance changed significantly in the R. conorii-infected human umbilical vein endothelial cel

46 The kinetics of development of antibodies to R. conorii determined by immunoblotting revealed antibod

47 immune responses of vascular endothelium to R. conorii infection.

48 Immunity to R. conorii after transfer of DCs was associated with up-

49 Transformed R. conorii stably maintains this plasmid in infected cel

50 Interestingly, plasmid-transformed R. conorii was readily observed both in endothelial cell

51 -treated and polyclonal Fab antibody-treated R. conorii.

52 Unlike wild-type R. conorii, pso mutants cannot elicit bactericidal antib

53 factor at 56 degrees C compared to R. typhi, R. conorii, and R. honei.

54 ed to inactivate O. tsutsugamushi, R. typhi, R. conorii, and R. honei.

55 acrophage-like cell lines were infected with R. conorii that had been exposed to polyclonal antibodie

56 esponse to antigen-specific stimulation with R. conorii.