ライフサイエンスコーパス: rosetting

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1 parasitemia were not correlated with P vivax rosetting.

2 rum malaria through the mechanism of reduced rosetting.

3 rough the mechanism of reduced P. falciparum rosetting.

4 dilution of hyaluronic acid had no effect on rosetting.

5 line phosphatase binding assays, and in situ rosetting.

6 Plasmodium falciparum rosetting, a parasite virulence phenotype associated wit

7 Both rosetting and cytoadherence are mediated by the parasite

8 Rosetting and cytoadherence have been widely studied as

9 e have mapped the region of CR1 required for rosetting and demonstrated that the CR1-dependent rosett

10 peripheral blood cells obtained using immune rosetting and separation of progenitors was developed to

11 phorin A-specific antibody binding, CHO cell rosetting, and P falciparum invasion.

12 Sequestration and rosetting are key determinants of Plasmodium falciparum

13 ed predominantly toward nonmalignant T cells rosetting around Reed-Sternberg cells provided meaningfu

14 ernberg cells and by most polyclonal T cells rosetting around Reed-Sternberg cells.

15 Using an antigen-specific rosetting assay and a mFc alpha R-expressing cell line,

16 A dilution of BSM but not PSM inhibited the rosetting assay by 17% (.2 mg/mL), 33% (1 mg/mL), and 53

17 e all tested for inhibitory potential in the rosetting assay.

18 eF did not impair its ability to inhibit the rosetting assay.

19 d immunosorbent assay, flow cytometry, and a rosetting assay.

20 Rosetting assays using CD236R knockdown normocytes deriv

21 with soybean lectin and by sheep-erythrocyte rosetting before transplantation.

22 ibility that C3b could be an intermediary in rosetting, bridging between the infected erythrocyte and

23 CD35; C3b/C4b receptor) have greatly reduced rosetting capacity, indicating an essential role for CR1

24 ther than reticulocytes, preferentially form rosetting complexes, indicating that this process is unl

25 Here we report that the parasite ligand for rosetting in a P. falciparum clone is PfEMP1, encoded by

26 They also show impaired rosetting interactions with non-parasitized erythrocytes

27 Rosetting is more common in vivax than falciparum malari

28 ting and demonstrated that the CR1-dependent rosetting mechanism occurs commonly in P. falciparum iso

29 ed cell sorting (MACS) and sheep erythrocyte rosetting methods, and the quality of cell fractions was

30 Although rosetting occurs in all causes of human malaria, most da

31 3 and anticapsular monoclonal antibodies and rosetting of fluorescent microspheres coated with anti-C

32 The CD32A-dependent rosetting of fMLP-activated normal neutrophils also incr

33 nstrated centrilobular cholestasis and focal rosetting of hepatocytes, consistent with a cholestatic

34 ment receptor 1 (CR1) has been implicated in rosetting of uninfected red blood cells to Plasmodium fa

35 s separate entities; however, the ability of rosetting P. falciparum strains to cytoadhere has receiv

36 Rosetting phenomenon has been linked to malaria pathogen

37 the preferential transcription of R29var in rosetting R29 parasites, a parasite line in which the A4

38 cells were CD25(-) provided that associated rosetting T cells expressed CD25.

39 ic peptide, increased the CD32A-dependent EA rosetting to 58%.

40 Rosetting to P vivax asexual and sexual stages was evide

41 In the same sample set, P. falciparum rosetting was reduced in parasite isolates from group O

42 cytoadherence of IT/R29 IE is distinct from rosetting, which is primarily mediated by NTS-DBL1alpha

43 on of individual cells based on differential rosetting with microspheres functionalized with monoclon

44 was induced by thrombin-activated platelets rosetting with neutrophils and was inhibited by anti-P-s

45 Surface IgM+ (sIgM+) B cells rosetting with TT-coated beads produced anti-TT IgM, IgG

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