Title of article :
Immunophenotype and functions of fetal baboon bone-marrow derived dendritic cells
Author/Authors :
Awasthi، نويسنده , , Shanjana and Cropper، نويسنده , , Jodie، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Pages :
10
From page :
31
To page :
40
Abstract :
Dendritic cells (DCs) are unique antigen-presenting cells that can take up pathogens, pathogens-derived and stress-antigens and stimulate antigen-specific immune response. Here we investigated the immunobiology of fetal DCs and compared their phenotype and activation status against infectious stimuli with those of young and adult baboons. The DCs were obtained from femoral bone-marrow (BMDCs) of fetus (140 and 175 days of gestation), young (4–5 years old) and mature adult (10–35 years old) baboons. The cells were cultured in the presence of GM-CSF and IL-4. To study phagocytic ability of BMDCs, the cells were harvested on 6th day and incubated with fluorescent-labeled Escherichia coli bioparticles. The BMDCs were also treated with E. coli O111:B4 lipopolysaccharide (LPS) for 24 h and changes in expression of cell-surface markers and IL-12 were studied using distinct immunoassays. We found that the phenotype and morphology of BMDCs from fetal, young and adult baboons were similar and showed increased expression of HLA-DP, DQ, DR and T cell co-stimulatory molecules upon LPS treatment. However, significant differences were observed in phagocytic activity and IL-12 secretion among BMDCs from these sources. The ability of fetal baboon BMDCs to phagocytose E. coli bioparticles was significantly lower and they secreted lower level of LPS-stimulated IL-12 as compared to the BMDCs from adult baboon. These results suggest that compared to adult BMDCs, fetal baboon BMDCs are less efficient in mounting immune response against Gram-negative bacterial stimuli.
Keywords :
dendritic cells , Cell-surface molecules , cytokine , Phagocytosis
Journal title :
Cellular Immunology
Serial Year :
2006
Journal title :
Cellular Immunology
Record number :
1857227
Link To Document :
بازگشت