Implication of delayed TNF-alpha exposure on dendritic cell maturation and expansion from cryopreserved cord blood CD34+ hematopoietic progenitors.

Most currently used systems for dendritic cell (DC) production from progenitors entail tumor necrosis factor alpha (TNF-alpha) at the onset of cell culture, based on the notion that TNF-alpha might be required in the early stages of DC development. To optimize conditions for DC expansion from cryopreserved cord blood (CB) CD34+ hematopoietic progenitors, we took a dynamic approach to define the timing of TNF-alpha exposure to the culture. We cultured cord blood CD34+ cells in RPMI-1640 with 10% human AB plasma, stem cell factor (days 1-6), granulocyte-macrophage colony-stimulating factor (days 1-18), interleukin-4 (days 6-18) and varying schedules of TNF-alpha (0-144 h after thawing).

[Inhibition of lectin induced peripheral blood lymphocyte proliferation by colorectal cancer extract: a preliminary report of three cases].

Background: Tumor infiltrating lymphocytes (TIL) in colorectal cancer are a manifestation of local, cell mediated immune response to the malignant tumor. Tumor progression is due to impairment of the host ability to control tumor growth. Several studies suggested possible causes for such impairment, however, the precise factor(s) underlying such malfunction is uncertain.

Plasminogen activator inhibitor-1 promotes formation of endothelial microparticles with procoagulant potential.

Background: Endothelial dysfunction is emerging as a common denominator for diverse and highly prevalent cardiovascular diseases. Increased level of plasminogen activator inhibitor-1 (PAI-1) and procoagulant activity have been recognized as hallmarks of endothelial dysfunction. This study was aimed at investigating cellular actions of PAI-1 and a potential link between PAI-1 and procoagulant state.