Haemopoietic stem cells: spleen colony-forming cells are normally actively proliferating
Jazyk angličtina Země Anglie, Velká Británie Médium print
Typ dokumentu časopisecké články
- MeSH
- antibakteriální látky farmakologie MeSH
- buněčné dělení účinky léků MeSH
- buňky produkující protilátky účinky léků MeSH
- cyklofosfamid farmakologie MeSH
- cyklosporiny farmakologie MeSH
- gnotobiologické modely MeSH
- hematopoetické kmenové buňky cytologie MeSH
- imunosupresivní léčba MeSH
- myši inbrední C57BL MeSH
- myši inbrední CBA MeSH
- myši MeSH
- polymyxin B farmakologie MeSH
- slezina cytologie MeSH
- T-lymfocyty účinky léků MeSH
- thymektomie MeSH
- transplantace kostní dřeně MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- antibakteriální látky MeSH
- cyklofosfamid MeSH
- cyklosporiny MeSH
- polymyxin B MeSH
The haemopoietic stem cells forming spleen colonies (CFU-S) had on average 30 to 40% of cells engaged in the DNA synthesis in normal mice continuously over 4 years. A majority of experiments aimed at the suppression of the CFU-S proliferation, which included suppression of the T-lymphocytes by means of cyclosporin A or by adult thymectomy, administration of antibacterial and antifungal agents and maintainance of mice in a sterile environment, suppression of antibody-producing cells by a successive administration of the bacterial lipopolysaccharide and cyclophosphamide and attempts to increase the total number of CFU-S in the body through massive transfusions of bone marrow cells or by grafting plugs of the bone marrow under the kidney capsulae, have not been sufficiently effective. A transient suppression of CFU-S proliferation occurred during recovery of the haemopoietic tissue from damage caused by cyclophosphamide. The results support the view that changes in CFU-S numbers and in the proportion of them in DNA synthesis may be positively correlated when CFU-S numbers fluctuate physiologically about their normal values. The failure to manipulate the CFU-S proliferation rate easily suggests that proliferation of these cells may not be under a strong 'switch on - switch off' control.
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