Objective To study the role of cytidine-phosphate-guanosine oligodeoxynucleotide(CpG ODN) on the development of Plasmodium liver stage.Methods Plasmodium yoelii BY265 18S rRNA was cloned,and the TaqMan real-time PCR was established on P.yoelii BY265 18S rRNA and mouse GAPDH as quantitative analysis model.The model was tested by the level of liver Plasmodium load with the liver cDNA in BALB/c mice infected by salivary gland sporozoites for 42 hours.Twelve BALB/c mice were randomly divided into CpG group,CpG control group and PBS control group which were injected respectively by ODN1826 30 ?g,ODN1826 control 30 ?g and 0.01 mol/L PBS 200 ?l via vena caudalis.Twenty-four hours later,each mouse was inoculated with 100 sporozoites.Mice were sacrificed in 42 hours after infection,and the liver load of Plasmodium was analyzed by TaqMan real-time PCR.Results The cloned Py BY265 18S rRNA gene showed 98% similarity to Py 17XNL.The quantitative analysis model consisted by 18S rRNA and GAPDH showed positive correlation between the level of liver Plasmodium load and the sporozoite inoculation dose to mice.The Plasmodium load in CpG ODN pre-treated mice was reduced to one fifth of the control group(0.28/1.33)(P

Objective: To investigate the effects of normal and pathological bone marrow stromal cells(BMSC) on the proliferation and apoptosis of K562 cells in separated culture and contact culture.Methods: On 2,4,7 and 12 d after culture,the growth of K562 cells was observed under optical microscope;the apoptosis of K562 cells was detected by TUNEL. Results: the growth of K562 cells on CML BMSC in contact culture was faster than the else.The growth of K562 cells in contact culture was significantly faster than that in separated culture after 7 d(P

Objective To explore the feasibility of mobilization circulating MSCs by G-CSF and observe the repairing effect of G-CSF mobilization in severe mouse traumatic brain injury(TBI) model.Methods MSCs-derived bone marrow and peripheral blood(PB) were cultured and its CFU-F were counted after mobilization by G-CSF.At 2,24,48,96,120,144,192,264,336 h after severe TBI in mice was establish,the neurobehavior of mice was measured by neurological examination and motor functional test,and mortality rate and pathologic changes were analyzed.Results MSCs-derived PB were successfully cultured.The CFU-F of mobilization group increased significantly than that of control group(P

OBJECTIVETo investigate the role of natural killer-22 (NK-22) cells in the synovial fluid in the proliferation of fibroblast-like synoviocytes (FLS) in patients with rheumatoid arthritis (RA) and explore the possible signal pathway involved.

METHODSNK-22 cells in the SF of RA patients were sorted by flow cytometry. NK-22 cells were cultured for two weeks and the purity was detected by flow cytometry before stimulation with 20 ng/ml phorbol 12-myristate 13-acetate and 0.5 µmol/L ionomycin for 4 h. The level of interleukin-22 (IL-22) in the culture medium supernatant was then measured with ELISA. The proliferation of FLS in the presence of the culture supernatant of NK-22 cells was assessed with MTT assay at 24, 48 and 72 h, and the effect of IL-22 antibody on FLS proliferation was also observed. Real-time PCR and Western blotting were used to detect Stat3 mRNA and p-Stat3 protein levels, respectively, in the FLS exposed to rhIL-22 and AG490.

RESULTSNK-22 cells were successfully sorted by flow cytometry with a purity exceeding 90%. The levels of IL-22 in the supernatant of NKp44(+)NK cell culture averaged 1273.42∓254.48 pg/ml. The FLS proliferated rapidly 24, 48, and 72 h after the addition of culture supernatant of NK-22 cells (P<0.05). IL-22 antibody obviously inhibited the proliferation of FLS induced by NK-22 cell culture supernatant (P<0.05). Exposure of the FLS to rhIL-22 obviously increased cellular Stat3 expression levels, which were significantly lowered by the addition of AG490 (P<0.05).

CONCLUSIONNK-22 cells in the SF of RA patients can produce high concentrations of IL-22 to promote the proliferation of FLS through the STAT3 signal pathway.

Arthritis, Rheumatoid ; metabolism ; Cell Proliferation ; Cells, Cultured ; Fibroblasts ; cytology ; Humans ; Interleukins ; metabolism ; Killer Cells, Natural ; cytology ; metabolism ; STAT3 Transcription Factor ; metabolism ; Signal Transduction ; Synovial Fluid ; cytology ; Synovial Membrane ; cytology

Toxoplasma gondii is an obligate intracellular parasite and causes serious harm to human and ani-mal health.In recent years,a large amount of research has been conducted on the immunological mechanism of toxo-plasmosis,especially in the immune privileged regions of the host,such as brain,eyes,and placenta.This review summaries the immunological mechanism required for resistance to toxoplasmosis,which may provide a valuable ref-erence for the diagnosis,treatment,and prevention studies.